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https://en.wikipedia.org/wiki/Toxicant


This page is about artificial and natural toxic substances. For naturally occurring organic poisons, see Toxin.
Diagram showing how mercury can penetrate the food chain in various ways.
Mercury can penetrate the food chain through various ways.[1]

A toxicant (pronounced tɒksɪkənt[2]) is any toxic substance that is not safe to a living organism due to its negative impact on tissues, organs, or biological processes, including the reproductive system.[3] Toxicants can be poisonous[4] and they may be artificial or naturally occurring.[5] The majority of toxicants do not originate from within the bodies of the subjects that are affected and tend to gravitate towards lipids.[4] Thus, they can move through the lipid membrane of cells and accumulate to toxic concentrations.[4]

The different types of toxicants[4] can be found in the air, soil, water, or food.[6] Humans can be exposed to environmental toxicants.[7] For example, exposure to small amounts of the environmental toxicant cadmium negatively impacts human male and female reproduction.[8] Environmental toxicants are associated with a diverse array of unfavorable persistent health effects across different biological systems, with detrimental health and economic impacts for people and society.[9] While exposure to environmental toxicants and pregnancy consequences are limited, there are some substantiated connections between toxicants and unfavorable pregnancy consequences such as mercury and neurological harm.[10]

Tobacco cigarette smoke contains many disease-inducing toxicants.[11] E-cigarette aerosol also contains many of the toxicants found in traditional cigarettes, including formaldehyde, cadmium, and lead, typically at lower levels.[12] Nicotine is potentially harmful to non-users[13] and the evidence shows that the utmost caution should be exercised when it concerns children being exposed to developmental toxicants (e.g., nicotine).[14] Epigenetic modifications may be triggered by the environment (e.g., toxicants).[15] Mounting evidence, primarily in animals, suggests environmental exposures may generate or perpetuate altered health outcomes across one or more generations.[16] Some effects of environmental exposures can be transmitted across generations via changes to the sequence of germline DNA.[16]

By contrast, a toxin is a poison produced naturally by an organism (e.g., plant, animal, insect).[17] The 2011 book A Textbook of Modern Toxicology states, "A toxin is a toxicant that is produced by a living organism and is not used as a synonym for toxicant—all toxins are toxicants, but not all toxicants are toxins. Toxins, whether produced by animals, plants, insects, or microbes are generally metabolic products that have evolved as defense mechanisms for the purpose of repelling or killing predators or pathogens."[18]

Definition

A toxicant is any toxic substance that is not safe to a living organism due to its negative impact on tissues, organs, or biological processes, including the reproductive system.[3] Toxicants can be poisonous[4] and they may be artificial or naturally occurring.[5] The majority of toxicants do not originate from within the bodies of the subjects that are affected and tend to gravitate towards lipids.[4] Thus, they can permeate the lipid membrane of cells and accumulate to toxic concentrations.[4]

Occurrence and effects

Overview

Structural formula of formaldehyde
Formaldehyde structure

There are different types of toxicants.[4] and they can be found in the air, soil, water, or food.[6] Humans can be exposed to environmental toxicants.[7] Environmental toxicants are associated with a diverse array of unfavorable persistent health effects across different biological systems, with detrimental health and economic impacts for people and society.[9]

Most toxicants that pollute the environment are artificial (man-made), but some can be created by natural events.[5] For example, wildfires are a significant source of contamination in the air and water because they disperse polycyclic aromatic hydrocarbons into the environment.[5] Other routes of exposure to polycyclic aromatic hydrocarbons include ingestion, inhalation, and skin contact in workplace settings, inhaling outdoor and indoor air, and consuming food that contain polycyclic aromatic hydrocarbons.[19] Because of the heating or cooking of food at high temperatures such as grilling, smoking, toasting, roasting, and frying, food can become contaminated with polycyclic aromatic hydrocarbons.[20]

Traditional and modern tobacco products and impact

Tobacco cigarette smoke contains many disease-inducing toxicants, and this daily nicotine-addicted smoking results in disability, disease, and more than 400,000 deaths in the US every year.[11] Tobacco use kills more than eight million people worldwide each year; this number comprises about seven million as a result of direct tobacco use and about 1.2 million passive smokers.[13] Furthermore, tobacco kills up to half its users and is the cause of nearly 90% of all lung cancers.[21] A multitude of inner-city environmental pollutants may trigger the onset of asthma, which includes tobacco smoke.[22] Like cigarette smoke, cannabis smoke contains toxicants.[23] These are, but not limited to, several aromatic amines, volatile organic compounds, and several polycyclic aromatic hydrocarbons.[24]

External video
The past, present and future of nicotine addiction

E-cigarette aerosol also contains many of the toxicants found in traditional cigarettes, including formaldehyde, cadmium, and lead, typically at lower levels.[12] However, the later-generation and "tank-style" e-cigarettes with a higher voltage (5.0 V[25]) may generate equal or higher levels of formaldehyde compared to smoking.[26] Formaldehyde is an environmental neurotoxicant associated with neurodegeneration in humans.[27] The Juul aerosol contains several of the same toxicants that are detected in tobacco smoke, though generally at notably lower percentages.[28] Flavorings, as part of a mixture in the e-liquid, may be a significant source of e-cigarette aerosol toxicants.[29] The emissions of a heated tobacco product contains toxicants[30] such as tobacco-specific nitrosamines[31] and smoke.[32] Many toxicants including plasticizers have been found in Illegally sold tetrahydrocannabinol vaping products that were associated with an outbreak of vaping-induced lung injuries in 2019 and 2020.[33]

Vaping products and environmental toxicants exposure and lung cancer risk
Vaping products and environmental toxicants exposure and lung cancer risk[34]

Human exposure to environmental toxic substances with different mechanisms of action is a growing concern.[34] Even though tobacco smoking is a potent lung carcinogen, a significant percentage of lung cancer mortality occurs in non-smokers.[34] Other risk factors besides smoking can contribute to 15–25% of all lung cancer of non-smokers; however, its epidemiology is poorly established.[34] It is recognized that various chemicals in environmental contexts have been proposed to affect health.[34] Exposure to known and probable respiratory carcinogens, such as metals and organic toxicants, is an essential enhancer of carcinogenesis.[34] Chronic pulmonary inflammation is a significant risk factor for lung cancer tumorigenesis.[34] The association between environmental toxicants and lung cancer in epidemiological evidence is poorly established.[34] However, numerous experimental investigations have demonstrated that several substances, such as heavy metals, ionizing radiation, pesticides, dust and fibers, household coal, arsenic, asbestos, and polycyclic aromatic hydrocarbons, can cause cellular and molecular changes that can facilitate the development of cancer.[34] The lifelong exposure to various toxicants, dosing, confounding variables, and human physiological diversity are essential issues in lung cancer development.[34] Recently, as of 2023, the adverse effects of environmental toxicants on the lungs have been an area of intense investigation.[34]

Co-exposure to various lung carcinogens could play a more synergistic or additive role in lung carcinogenesis than single carcinogen exposure.[34] Nowadays, as of 2023, the prevalence of vaping is on the rise accompanied by polluted air and contaminated environment.[34] Additionally, the aerosol from vaping contains several carcinogenic compounds that contribute to environmental contamination.[34] With the rapid increase in e-cigarette users worldwide, second-hand exposure to e-cigarettes aerosols has become a serious public health concern.[34] It is proven that both smokers and second-hand exposure who live in contaminated environment are more prone to develop lung cancer than others.[34] The incidence of lung cancer is rising, as of 2023, among non-smokers or second-hand exposure which could be attributed to exposure to environmental carcinogenic compounds.[34] Importantly, more than 70% of inhaled E-cigarette aerosols are eventually exhaled, which may negatively affect the user's health.[34] The aerosol from vaping contains several carcinogenic compounds that increase the risk of lung cancer in both user and from second-hand exposure.[34] Vaping aerosol and waste products share in environmental contamination and consequently increase the risk of lung cancer.[34] Exposures to specific environmental toxicants, either from vaping or other resources such as air pollution, heavy metals, and asbestos, have been reported to have a negative impact on pulmonary function and enhance lung carcinogenesis.[34] The high levels of indoor air pollutants produced by e-cigarettes are raising alarms for public health.[34] Nicotine is potentially harmful to non-users.[13]

Figure shows relationship between potential effects of cigarette smoke exposure and COVID-19 on the developing lungs. This may result in exacerbating common pediatric lung diseases – i.e., chronic lung disease of prematurity, asthma, and wheezing disorders. Underlying processes of inflammation and tissue remodeling are enhanced by chronic cigarette smoke exposure. SARS-CoV-2 infection triggers an acute inflammatory response that may compromise the respiratory function of these vulnerable patients. Longitudinal clinical data are needed to confirm whether these factors have an additive effect that leads to more severe COVID-19 manifestations and/or long-term consequences in terms of lung function decline.
Figure shows relationship between potential effects of cigarette smoke exposure and COVID-19 on the developing lungs.[35] This may result in exacerbating common pediatric lung diseases – i.e., chronic lung disease of prematurity, asthma, and wheezing disorders.[35] Underlying processes of inflammation and tissue remodeling are enhanced by chronic cigarette smoke exposure.[35] SARS-CoV-2 infection triggers an acute inflammatory response that may compromise the respiratory function of these vulnerable patients.[35] Longitudinal clinical data are needed to confirm whether these factors have an additive effect that leads to more severe COVID-19 manifestations and/or long-term consequences in terms of lung function decline.[35]

Cigarette smoke derives from burning tobacco products (e.g., cigarettes, cigars, and pipes) or smoke that has been exhaled by a person smoking.[35] Second-hand smoke exposure represents the typical source of cigarette smoke exposure in children.[35] In the US, more than 128 million non-smokers are exposed to second-hand smoke at any age.[35] Children, however, have a higher risk of second-hand smoke exposure compared to the non-smoking adult population because of their frequent exposure from household members.[35] The World Health Organization estimates that around 700 million children – almost half of the world's pediatric population – have significant exposure to second-hand smoke.[35] Among the environmental factors that affect the developing lung, cigarette smoke is certainly one of the most prevalent, despite being preventable.[35] Repeated hits of cigarette smoke exposure and pulmonary infections may certainly exacerbate preexisting chronic pediatric pulmonary disease or lead to the development of pulmonary disease in at-risk children.[35]

Detrimental effects on respiratory function are common in children exposed to second-hand smoke.[35] A 2011 systematic review and meta-analysis of 60 studies concluded that passive smoke exposure increases the risk of pediatric lower respiratory tract infections, with the risk becoming even greater in cases where both parents smoke.[35] Not only does second-hand smoke exposure facilitate the onset of respiratory diseases and infections, but it may also exacerbate symptoms of pre-existing diseases such as asthma.[35]

Cigarette smoke exposure results in three main impacts: epithelial to mesenchymal transformation, loss of epithelial barrier function (which may increase susceptibility to infection), and chronic inflammation and immune dysfunction.[35] In addition, smoking increases angiotensin-converting enzyme 2 (ACE2) expression, which is a key entry point for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), thus potentially increasing susceptibility to infection.[35] COVID-19 also results in significant inflammation and cytokine response.[35] Synergy between cigarette smoke exposure and SARS-CoV-2 may occur in activation of pro-inflammatory mediators, such as TNF-α, IL-1β, IL-6, and other mediators that may result in cytokine storm, pronounced inflammatory state, and immune dysfunction.[35]

Human activities and impact

Many human activities cause a double burden, on health and on the environment. A few examples are as follows: Air pollution causes greenhouse gas emissions and several human diseases (left). Food production and trades are involved in loss of biodiversity, greenhouse gas emissions, and human diseases such as zoonoses or excess cancer and cardiovascular diseases (right). Intersectoral policies can contribute to the achievement of several Sustainable Development Goals.
Many human activities cause a double burden, on health and on the environment.[36] A few examples are as follows: Air pollution causes greenhouse gas emissions and several human diseases (left).[36] Food production and trades are involved in loss of biodiversity, greenhouse gas emissions, and human diseases such as zoonoses or excess cancer and cardiovascular diseases (right).[36] Intersectoral policies can contribute to the achievement of several Sustainable Development Goals.[36]

An area of overlap between ill health, including cancer, and climate change is air pollution.[36] In 2016, the International Agency for Research on Cancer's Monograph Working Group concluded that outdoor air pollution is carcinogenic to humans (sufficient evidence), with particular focus on particulates.[36] Air pollutants associated with fossil fuel combustion have other well‐documented adverse human health effects beyond cancer (e.g., cardiovascular and respiratory diseases).[36] Changes in transportation, in particular an increase in the promotion of active transportation such as walking and use of bicycles, may reduce air pollution, while at the same time contributing to better health in several ways, by increasing physical activity and, thus, reducing the risk of obesity, diabetes, cancer, and cardiovascular disease. As an example, it has been estimated that clean energy policies in the United States could prevent 175 000 premature deaths by 2030 and 22 000 annually thereafter, and clean transportation could prevent 120 000 US premature deaths by 2030 and about 14 000 annually thereafter.[36] But, once again, the emission of air pollutants has also an important impact on climate: transportation overall contributes to 13% of all greenhouse gases.[36] Further, the impact of international trade of food on planetary and human health includes air pollution related to transportation, the ensuing climate changes, and land and water use in low‐income countries.[36]

Most heavy metals are toxicants.[37] Fish can contain environmental toxicants[38] such as methylmercury,[39] which is the most harmful form to people.[40] Mercury, including its various forms, is on the World Health Organization's top ten list of toxic chemicals of serious public health concerns.[41] Arsenic is a known toxicant[42] and can be found in rice originating from various areas of Asia, Europe, and the US.[43] Cadmium is an environmental toxicant and exposure to small amounts of it negatively impacts human male and female reproduction.[8] Although originally considered environmentally benign,[44] the possible adverse effects of the environmental toxicant tungsten to humans remains scant.[45] The toxicants Bisphenol A, arsenic, phthalates, perfluorinated compounds, bis(2-ethylhexyl) phthalate, and 2,3,7,8-Tetrachlorodibenzodioxin are frequently identified in the blood and urine in the Centers for Disease Control and Prevention’s National Health and Nutrition Examination Survey populations and assumed to also be frequently detected in the people in the US in general.[46]

While exposure to environmental toxicants and pregnancy consequences are limited, there are some substantiated connections between toxicants and unfavorable pregnancy consequences such as mercury and neurological harm.[10] The most frequent source of exposure in humans to the toxicant hydrogen sulfide is breathing in or consuming of polluted drinking water.[10] Minimal evidence suggests that negative pregnancy consequences are related to this exposure.[10] Air particulates, including but not limited to, dust, smoke, and fumes, are linked to adverse pregnancy results.[10] This includes reduced gestation, low birth weight, and lower fetal size.[10] Inhalation represents the most frequent source of exposure and consuming of dissolved particulates in water represents another source of exposure.[10] Exposure during pregnancy to environmental toxicants is a major concern.[9] International Federation of Gynaecology and Obstetrics, the American Society for Reproductive Medicine, the American Academy of Pediatrics, and the Endocrine Society support reducing exposure to environmental toxicants during pregnancy.[9]

Diesel exhaust contains toxicants.[47] Perfluoroalkyl and polyfluoroalkyl substances used in various consumer products[48] such as non-stick cookware[49] are potential fetal developmental toxicants.[50] Pesticides, benzene, and asbestos-like fibers such as carbon nanotubes are toxicants.[51] Possible developmental toxicants include phthalates, phenols, sunscreens, pesticides, halogenated flame retardants, perfluoroalkyl coatings, nanoparticles, e-cigarettes, and dietary polyphenols.[52] The evidence shows that the utmost caution should be exercised when it concerns children being exposed to developmental toxicants (e.g., nicotine).[14]

Exogenous and endogenous sources of human exposure to aldehydes
Exogenous and endogenous sources of human exposure to aldehydes[53]

Human exposure to aldehydes is implicated in multiple diseases including diabetes, cardiovascular diseases, neurodegenerative disorders (i.e., Alzheimer's and Parkinson's Diseases), and cancer.[53] Because these compounds are strong electrophiles, they can react with nucleophilic sites in DNA and proteins to form reversible and irreversible modifications.[53] These modifications, if not eliminated or repaired, can lead to alteration in cellular homeostasis, cell death, and ultimately contribute to disease pathogenesis.[53] They are ubiquitous in the environment, originating from man-made sources, as well as through natural processes.[53]

In industrialized areas, the majority of aldehydes are produced from motor vehicle exhaust (internal diesel engine combustion), which either directly yields aldehydes or generates hydrocarbons, which are eventually converted to aldehydes by photochemical oxidation reactions.[53] Formaldehyde, acetaldehyde, and acrolein are significant contributors to the overall summed risk of mobile sources of air toxicants according to the United States Environmental Protection Agency.[53] Other sources of aldehydes include agricultural and forest fires, incinerators, and coal-based power plants.[53] Additionally, humans are exposed to aldehydes in residential and occupational settings where aldehydes are present in confined spaces due to the release of fumes from indoor furniture, carpets, fabrics, household cleaning agents, cosmetic products, and paints.[53] Aldehydes are also widely used as fumigants and for biological specimen preservation.[53]

Another major source of aldehyde exposure comes from cigarette smoke.[53] Mainstream tobacco smoke is composed of significant amounts of acetaldehyde as the major component, followed by acrolein, formaldehyde, and crotonaldehyde.[53] Similarly, popular devices such as e-cigarettes, which are advocated as safer alternatives to tobacco, have been found to generate high concentrations of aldehydes.[53] Aldehydes are also present in food and beverages (as flavorings), and in alcoholic drinks either as congeners or, in the case of acetaldehyde, as the oxidative by-product of ethanol.[53] Biotransformation is another source of aldehyde exposure.[53] This includes metabolism of a sizeable number of environmental agents, such as drugs, tobacco smoke, alcohol, and other forms of xenobiotics.[53] Excessive exposure to aldehydes can result in the disruption of a number of cellular functions, which can ultimately contribute to human diseases.[53]

Non-human activities and impact

Volcanic eruptions release large plumes of inorganic toxicants such as sulfur dioxide and carbon dioxide into the atmosphere.[5] Every year there are 10 to 40 volcanic eruptions.[54] Volcanic eruptions produce hazardous effects for the environment, climate, and the health of the exposed persons, and are associated with the deterioration of social and economic conditions.[54]

Their unfavorable effects depend on the distance from a volcano, on magma viscosity, and on gas concentrations.[54] The hazards closer to the volcano include pyroclastic flows, flows of mud, gases and steam, earthquakes, blasts of air, and tsunamis.[54] Among the hazards in distant areas are the effects of toxic volcanic ashes and problems of the respiratory system, eyes and skin, as well as psychological effects, injuries, transport and communication problems, waste disposal and water supplies issues, collapse of buildings and power outage.[54]

Further effects are the deterioration of water quality, fewer periods of rain, crop damages, and the destruction of vegetation.[54] During volcanic eruptions and their immediate aftermath, increased respiratory system morbidity has been observed as well as mortality among those affected by volcanic eruptions. Unfavorable health effects could partly be prevented by timely application of safety measures.[54]


https://pubmed.ncbi.nlm.nih.gov/?term=Volcanic+eruptions+and+health&size=200

Candles, perfumes, and cleaning products and impact

A flameless candle
A flameless candle

Scented candles have become increasingly popular, though they may not be without their own risks in terms of the release of pollutants into the atmosphere.[55] Flameless candles do not emit toxic chemicals into the air.[56]

The Human Ecology Action League reported that one in five people in the US are adversely affected by exposure to synthetic fragrances in perfumes and cleaning products.[55] Some individuals have a heightened sensitivity to chemicals that may be triggered by the presence of ambient volatiles chemicals.[55]


https://reviewed.usatoday.com/health/features/are-candles-bad-for-you-shop-non-toxic-options

Measurement and evaluation of gaseous and particulate emissions from burning scented and unscented candles

https://pubmed.ncbi.nlm.nih.gov/?filter=pubt.booksdocs&filter=pubt.meta-analysis&filter=pubt.review&filter=pubt.systematicreview&linkname=pubmed_pubmed&from_uid=33964641

Human health risk evaluation of selected VOC, SVOC and particulate emissions from scented candles

https://pubmed.ncbi.nlm.nih.gov/?filter=pubt.booksdocs&filter=pubt.meta-analysis&filter=pubt.review&filter=pubt.systematicreview&linkname=pubmed_pubmed_citedin&from_uid=24582651

Brain impact

Potential pathways by which inhaled particles affect the brain
Potential pathways by which inhaled particles affect the brain[57]

A great deal of scientific research demonstrates that air pollution exposure can lead to harmful health effects related to the lungs and heart.[57] Studies show that air pollution can have harmful effects on the brain.[57] Research findings about associations between air pollution and negative effects on the brain are just beginning to emerge, therefore, definite conclusions cannot be made as of 2018.[57]

Studies have compared children living in Mexico City, an area with high air pollution, versus those living in less polluted regions of the country.[57] The Mexico City children had poorer brain health than the other children, including the following: Breakdown of the brain’s protective layer; Changes in the brain resembling the early stages of Alzheimer's disease; and Poorer performance on standardized psychological tests. Mexico City has high outdoor pollutant levels, but it is not clear what pollutants, or other factors, might cause these health problems.[57]

Studies that exposed animals to ultrafine particulate matter (ultrafine particulate matter, particles less than 0.1 micrometers in diameter) showed the following: Inhaled particles can travel through a nerve running from the nasal cavity into the brain, bypassing the lungs; ultrafine particulate matter carried in the bloodstream can pass through the barrier that normally protects the brain; and Chemical markers of brain inflammation can increase.[57] Thus, air pollutants can affect the brain directly and indirectly, and are associated with potentially harmful effects.[57] These findings strengthen the case for inhaled pollutant-related brain impacts.[57]

Animals exposed to particulate matter or diesel particulates demonstrated: Poorer performance in mazes, and other learning and memory problems; and Behaviors resembling human anxiety, depression, and impulsiveness.[57] In humans, emerging evidence suggests links between air pollution and harmful brain effects in the elderly.[57]

Two studies showed associations between air pollution and dementia: A study in Ontario, Canada found that the risk of dementia increased the closer people lived to major roadways.[57] A study of US women showed higher risk of cognitive decline and dementia for those exposed to levels of fine particulate matter (particulate matter2.5, particles less than 2.5 micrometers in diameter) above the national standard.[57] Fine particles are more dangerous because they can get into the deep parts of your lungs — or even into a parson's blood.[58]

Multigenerational effects

See also: Epigenetic effects of smoking, Smoking and pregnancy, Women and smoking, and Environmental toxicants and fetal development
Figure shows the multigenerational effects of intergenerational and transgenerational inheritance. Depiction of inheritance patterns from the parent (F0) generation to the child (F1), grandchild (F2), and great-grandchild (F3) in humans and animals. An exposure in F0 can directly affect the developing fetus (F1) and the germ cells in F2; therefore, both routes of transmission are considered intergenerational. Transgenerational effects may be observed beginning with the F3 generation.
Figure shows the multigenerational effects of intergenerational and transgenerational inheritance.[16] Depiction of inheritance patterns from the parent (F0) generation to the child (F1), grandchild (F2), and great-grandchild (F3) in humans and animals.[16] An exposure in F0 can directly affect the developing fetus (F1) and the germ cells in F2; therefore, both routes of transmission are considered intergenerational.[16] Transgenerational effects may be observed beginning with the F3 generation.[16]

Environmental exposures (as well as psychosocial stressors and nutrition) are potentially important influences that may impact health outcomes directly or via interactions with the genome or epigenome over generations.[16] While there have been clear successes in large-scale human genetic studies in recent decades, there is still a substantial amount of missing heritability to be elucidated for complex childhood disorders.[16] Mounting evidence, primarily in animals, suggests environmental exposures may generate or perpetuate altered health outcomes across one or more generations.[16]

Some effects of environmental exposures can be transmitted across generations via changes to the sequence of germline DNA.[16] It is also thought that environmental exposure effects can be transmitted across generations via epigenetic modifications of germline DNA.[16] When nonpregnant individuals are exposed, the earliest transgenerational effects that could be assessed are in their grandchildren; when pregnant females are exposed, the earliest transgenerational effects that could be assessed are in their great-grandchildren.[16]

While evidence in support of transgenerational transmission exists in animal models, evidence in humans is virtually nonexistent, in part because of logistic, financial, and ethical hurdles that limit epidemiologic studies spanning multiple generations.[16] Many common environmental exposures are not restricted to a single-generation in humans, making it difficult to distinguish between inherited and current effects.[16] Major challenges to demonstrating that epigenetic mechanisms are specifically responsible for transgenerational effects include the need to evaluate epigenetic marks across multiple tissues, the difficulties in ruling out confounding effects of genetic, ecological, and sociocultural factors, and the inability to control completely the effects of other environmental influences.[16]

In males, because sperm are produced continuously in the testes from puberty onward, current exposures are often considered as potential triggers of both genetic and epigenetic changes.[16] A number of health conditions, behaviors, and environmental exposures in men have been associated with sperm DNA fragmentation, including obesity, smoking, varicocele, sexually transmitted infection, chemotherapy or radiotherapy, paracetamol, air pollution, and a variety of endocrine-disrupting chemicals.[16] In turn, sperm DNA fragmentation has been linked to male factor infertility, miscarriage, and reduced live birth rate after in vitro fertilization.[16] Male offspring of sub-fertile fathers who used intracytoplasmic sperm injection to conceive were at increased risk of poor semen quality and likely to have genetic abnormalities related to azoospermia, indicating the potential heritability of subfertility that may result from environmentally-induced alterations to germline DNA.[16]

Epigenetic mechanisms have also been proposed to explain the transmission of obesity from father to child.[16] Rodent studies indicate that, in addition to diet and exercise, paternal stress and exposure to endocrine-disrupting chemicals may affect offspring health and behavior via epigenetic pathways.[16] One of the most notable causes of sperm DNA fragmentation is oxidative stress.[16] Sperm are particularly vulnerable to genetic damage due to oxidative stress because sperm heads, which are filled with tightly packed chromatin, lack cytoplasm that contains the enzymes necessary for DNA repair.[16] oxidative stress may also affect the sperm epigenome, as some studies have shown hypoxia to be associated both with impairments in spermatogenesis and alterations in DNA methylation.[16] In general, it is theorized that OS-mediated sperm DNA fragmentation and/or epigenetic changes may underlie observed associations of a wide variety of paternal environmental and lifestyle factors with birth defects and childhood diseases.[16]

A growing body of literature supports associations between prenatal exposures and epigenetic modifications in children.[16] Epigenetic processes, such as CpG methylation and chromatin remodeling, are highly regulated during embryogenesis to ensure proper development.[16] Disruption of these mechanisms is of interest to child health researchers because they facilitate key developmental events, including placental and fetal growth, genomic imprinting, and cell differentiation.[16] While epigenetic modifications demonstrate plasticity during development, they also can remain stable, biologically embedding the effects of periconceptional exposures within offspring.[16] Environmental perturbation of epigenetic mechanisms can therefore change gene expression and result in altered outcomes, whether beneficial or adverse, at birth or later in life.[16] Nonetheless, studies that demonstrate epigenetic modifications that mediate the relationship between periconceptional exposures and child health using formal or causal mediation frameworks are generally lacking.[16]

Epigenetic modifications may be induced by prenatal exposures and can be inherited intergenerationally, escaping the major waves of epigenetic reprogramming that occur during fertilization and gametogenesis.[16] One hypothesized molecular mechanism for bypassing the DNA methylation reprogramming wave is through small regulatory RNAs, sequentially generated in parental somatic tissues, packaged in extracellular vesicles, and delivered to early embryos, where they ultimately drive a global reprogramming of genome expression.[16] Other means of escaping the early embryonic reprogramming are evidenced by CpG loci adjacent to intracisternal-A-particle elements or telomeric regions.[16] Single-generation epigenetic effects may also occur when exposures directly affect the developing somatic tissue postfertilization.[16] Single-generation effects have been investigated primarily in relation to maternal factors, including diet, environmental chemical exposure, cardiometabolic disorders, gut microbiota, and mental health, Paternal preconception diet and exposure to drugs, toxicants, and endocrine-disrupting chemicals have also been associated with epigenetic modifications among children.[16]

Numerous animal studies have described non-genetic inheritance of phenotypes, including eye color, cancer, and prostate and kidney diseases.[16] Often, these phenotypes result from environmental exposures during the parent generation, such as to particulate matter, diet, stress, and endocrine-disrupting chemicals.[16] In animal studies, generations are labeled as F0 (the exposed original generation), followed by F1, F2, F3… for subsequent generations.[16] Because maternal F0 exposures that occur during pregnancy have the potential to affect the F1 fetus as well as the developing F1 gametes that give rise to the F2 grand offspring, only patterns of maternal transmission that extend to the F3 generation meet the stricter criteria for transgenerational inheritance.[16]

Human studies that document both intergenerational and transgenerational effects of environmental exposures on health outcomes are relatively rare.[16] Moderate evidence exists for transmission of asthma, allergy, and other respiratory diseases through the third-generation.[16] In the nationally representative Child Development Supplement to the Panel Study of Income Dynamics cohort of more than 2500 children, children with a grandparent with asthma had one and half times the odds of reported asthma.[16] Children with a parent and grandparent with asthma had over a four times the odds of reported asthma compared with those without a parental or grandparental history of asthma.[16] Studies such as these have implicated genetic risk factors or gene-environment interactions for inherited asthma risk across a generation, however, nonbiological explanations and interactions between genetic and non-genetic risk factors are also feasible.[16] For example, multiple generations of families living in low-socioeconomic neighborhoods with higher exposure burden and greater poverty may also explain or exacerbate asthma risk.[16]

Perhaps, the most well-studied environmental risk factor for asthma is tobacco smoke.[16] A number of cohort studies have begun to evaluate inter- and transgenerational asthma risk to cigarette-smoking exposure.[16] In a case-control study nested within the Children's Health Study in Southern California, grandmaternal smoking during pregnancy was associated with a two-fold increased odds of asthma in the grandchild.[16] If both the child's mother and grandmother smoked during pregnancy, the child had even higher odds of developing asthma compared with no exposure.[16] In the Norwegian Mother and Child Cohort Study, grandmaternal smoking during pregnancy was associated with 15% and 21% greater relative risk of child asthma at ages three and seven years, respectively, and 15% greater relative risk for dispensed asthma medications at age seven years.[16] Data from the Ageing Lungs in the European Cohorts Study found that grandmaternal smoking during pregnancy was associated with child asthma with nasal allergies.[16]

In comparison to these studies based on retrospective reporting, prospectively collected data from the Swedish National Board of Health and Welfare and Statistics Sweden registries demonstrated that children of age one to six years had increased odds of asthma or of wheeze or asthma if their grandmothers smoked during weeks 10–12 of pregnancy, regardless of maternal smoking history.[16] The odds of asthma were higher with greater cigarette exposure (10 + cigarettes/day vs. none: OR 1.23, 1.17–1.30).[16] Grandmaternal smoking was associated most robustly with child early persistent asthma compared with early transient and late-onset asthma.[16] In contrast, the English population-based Avon Longitudinal Study of Parents and Children did not find evidence of transmission of effects of grandmaternal smoking during pregnancy on child lung function, bronchial responsiveness, or doctor-diagnosed asthma.[16] Overall, these studies provide relatively strong epidemiological support for an association between grandmaternal smoking and child asthma outcomes.[16] Notably, because most of this research relied on retrospective reporting of exposures, unmeasured residual confounding, and potential recall bias may have influenced results.[16] For example, differences in maternal education, geographical and temporal trends in smoking patterns, income level, and race and ethnicity not sufficiently included in study samples or completely accounted for in covariate-adjusted models may contribute to some of the discrepancies in the results.[16]

A few studies have examined birthweight across three generations.[16] In the Uppsala Birth Cohort Multigenerational Study in Sweden, correlations between grandparent and grandchild birthweight were stronger along the maternal line; however, this finding did not account for maternal birthweight.[16] In the Aberdeen cohort, grandmother's birthweight was associated with child birth weight independent of maternal birth weight as well as prenatal and sociodemographic factors.[16] Overall, the data from these and other cohorts suggest that social, environmental, and metabolic factors experienced by grandparents influence their grandchildren's birthweight.[16] Whether these effects are mediated by epigenetic mechanisms is unknown.[16] In some cases, epigenetic modifications, such as DNA methylation, have been associated with birthweight in the F1 generation, but their persistence to the F2 generation or beyond has not been assessed.[16] Although the methylation patterns that are associated with birthweight persist into childhood, there is evidence that they may not persist into adulthood.[16] Therefore, transfer to the F2 generation is less likely, although possible, since these human studies do not assess the methylation of gamete cell DNA.[16] Methylation patterns at the PBX1 locus have been associated with birthweight in more than one cohort, but are not associated with others.[16] This discrepancy in the results is unfortunately common in intergenerational epigenetic studies and may be due to differences in the environmental exposures that establish the epigenetic patterns.[16]

Current data suggest that some of the intergenerational social influences on birth weight include education, geographical location, and other sociodemographic characteristics.[16] For example, grandparents' educational attainment and residential environment have been associated with grandchildren's birthweight.[16] In the Fragile Families and Child Wellbeing Study, having a grandfather with less than a high school education was associated with a 93-gram reduction in birth weight and a 59% increase in odds of low birthweight.[16] An examination of multiple social and biological factors within the Aberdeen Children of the 1950s study showed that both distal and proximal grandparental and parental life-course biological and social factors predicted child size at birth.[16] Inequalities in size at birth appeared to be generated largely via continuity of the social environment across generations, with inequalities in maternal early-life growth predicted by the grandparental social environment during the mother's early life.[16] Studies of the social influences of intergenerational effects on birthweight rarely address potential epigenetic mechanisms by which these exposures affect outcomes.[16]

Some data suggest that associations between grandparents' BMI and grandchildren's birthweight are mediated by maternal BMI.[16] There is evidence that smoking may have intergenerational effects on birthweight.[16] One study, which accounted for family clustering, found that birth weight was higher in children whose grandmother and mother both smoked during their pregnancies relative to children whose grandmother and mother both did not smoke during pregnancy.[16] This association was dependent on the grandmother's birth cohort: infants whose grandmothers were born between 1929 and 1945 experienced this effect, but infants whose grandmothers were born between 1904 and 1928 did not.[16] Other studies have also shown that the relation between grandmothers' smoking and children's birthweight is mediated by maternal smoking.[16] However, the pattern of the results of these studies is not consistent.[16] Notably, these analyses have been conducted across a number of different time periods, when the content of cigarettes and the intensity of their use were changing frequently.[16] Therefore, the transgenerational influence of this environmental exposure on birthweight, and any role for epigenetics, remains unclear.[16]

Numerous grandparental exposures have been linked to grandchild neurodevelopmental outcomes.[16] Existing studies have focused largely on associations with child-externalizing problems (e.g., aggression, rule-breaking).[16] In at least two studies, the association between grandparental smoking history or substance use and child-externalizing behaviors was mediated by parental psychological symptoms and tobacco use.[16] Other studies have examined transgenerational effects of smoking on attention-deficit/hyperactivity disorder and an autism-spectrum disorder.[16] An analysis of the Norwegian Mother and Child Cohort found that grandparental smoking during pregnancy had a similar magnitude of association with child attention-deficit/hyperactivity disorder diagnosis as maternal smoking during pregnancy.[16] These findings suggest that the association between maternal smoking during pregnancy and child attention-deficit/hyperactivity disorder may not be due to causal intrauterine effects, but rather reflect unmeasured confounding factors.[16]

Related terms

Toxin

A 1080 poison risk warning sign
A 1080 poison risk warning sign

By contrast, a toxin is a poison produced naturally by an organism (e.g., plant, animal, insect).[17] The 2011 book A Textbook of Modern Toxicology states, "A toxin is a toxicant that is produced by a living organism and is not used as a synonym for toxicant—all toxins are toxicants, but not all toxicants are toxins. Toxins, whether produced by animals, plants, insects, or microbes are generally metabolic products that have evolved as defense mechanisms for the purpose of repelling or killing predators or pathogens."[18]

The studies of toad toxins have demonstrated new perspectives for their pharmaceutical use, not only for treating cardiac failure, but also for other therapeutic purposes, for example, as anti-inflammatory, immunoregulatory, and anticancer compounds.[59] Although different groups of constituents may have diverse functions, it is well known now that bufadienolides, such as bufalin and cinobufagin, are considered as the main bioactive compounds in toad toxins.[59] Bufalin is a major compound in Chansu (processed toad toxins and dried venom from parotoid glands of the of the toad Bufo bufo gargarizans), HuaChanSu (water extracts from the skins of Bufo bufo gargarizans), as well as the toxins of other toad species, such as Rhinella marinus.[59] Bufalin inhibits tumor growth by inducing cell apoptosis through the intrinsic apoptotic pathway.[59] Although snake venom can be fatal, a variety of snake venom toxins have been identified as potentially helpful for more than a few things such as acting as a therapeutic agent[60] for fighting certain types of cancer[61] such as colorectal cancer.[62]

Sodium monofluoroacetate, also known as 1080, is a pesticide used extensively to kill pest specifies such as the fox.[63] This toxin is found naturally in nearly 40 species of Australian plants such as Acacia, Gastrolobium, and Oxylobium.[63] Sodium monofluoroacetate is also found in very small amounts in tea leaves and guar gum.[63] A 2005 review states, "As 1080 is one of the most toxic pesticides known, there is concern about its fate in the living and non-living environment, its toxic effects on non-target species, and the risks of secondary poisoning."[63]

While over 300 mycotoxins have been identified, six (aflatoxins, trichothecenes, zearalenone, fumonisins, ochratoxins, and patulin) are regularly found in food, posing unpredictable and ongoing food safety problems worldwide.[64] Among the mycotoxins, aflatoxins are considered the most toxic, with significant economic burden to agriculture.[64] Aflatoxin-producing fungi grow on a wide variety of foods such cereals (maize, rice, barley, oats, and sorghum), peanuts, ground nuts, pistachio nuts, almonds, walnuts, and cottonseeds.[64] Mycotoxins are unpredictable and unavoidable contaminants in foods and feeds worldwide.[64] These small chemicals represent an open challenge for food safety and pose a serious risk for human and animal health while also contributing to massive economic losses to the agriculture industry.[64]

Biocide

Biocides are classified as oxidizing or non-oxidizing toxicants.[65] Chlorine is the most used industrial oxidizing toxicant.[65] Chlorine is ubiquitously added to drinking water to disinfect it.[66] Non-oxidizing toxicants include isothiazolinones and quaternary ammonium compounds.[67]

Intoxicant

An intoxicant is a substance that intoxicates such as an alcoholic drink.[68] An intoxicant is a substance that impairs the mind and causes a person to be in a state varying from exhilaration to lethargy.[69]

References

  1. ↑ "How Does Mercury End Up in Your Food?". Ground Truth Alaska. 2025.
  2. ↑ "How to pronounce toxicant?". HowToPronounce. 2024.
  3. ↑ 3.0 3.1 Irina Pollard (30 November 2002). Life, Love and Children: A Practical Introduction to Bioscience Ethics and Bioethics. Springer Science & Business Media. pp. 29–. ISBN 978-1-4020-7294-9.
  4. ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 4.7 Stanley Manahan; Stanley E. Manahan (17 December 2009). Environmental Chemistry, Ninth Edition. CRC Press. pp. 629–. ISBN 978-1-4398-8247-4.
  5. ↑ 5.0 5.1 5.2 5.3 5.4 Francisco Sánchez-Bayo, Paul J. van den Brink, Reinier M. Mann (9 September 2011). Ecological Impacts of Toxic Chemicals. Francisco Sanchez-Bayo. pp. 6–. ISBN 978-1-60805-121-2.{{cite book}}: CS1 maint: multiple names: authors list (link)
  6. ↑ 6.0 6.1 Ernest Hodgson (20 September 2011). A Textbook of Modern Toxicology. John Wiley & Sons. pp. 88–. ISBN 978-1-118-21129-8.
  7. ↑ 7.0 7.1 Preston, Joshua D.; Reynolds, Leryn J.; Pearson, Kevin J. (2018). "Developmental Origins of Health Span and Life Span: A Mini-Review". Gerontology. 64 (3): 237–245. doi:10.1159/000485506. ISSN 0304-324X. PMC 5876086. PMID 29324453.
  8. ↑ 8.0 8.1 Kumar, Sunil; Sharma, Anupama (18 December 2019). "Cadmium toxicity: effects on human reproduction and fertility". Reviews on Environmental Health. 34 (4): 327–338. doi:10.1515/reveh-2019-0016.
  9. ↑ 9.0 9.1 9.2 9.3 Kahn, Linda G.; Trasande, Leonardo (October 2018). "Environmental Toxicant Exposure and Hypertensive Disorders of Pregnancy: Recent Findings". Current Hypertension Reports. 20 (10): 87. doi:10.1007/s11906-018-0888-5. PMC 9371848. PMID 30090982.
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  14. ↑ 14.0 14.1 England, Lucinda J.; Bunnell, Rebecca E.; Pechacek, Terry F.; Tong, Van T.; McAfee, Tim A. (August 2015). "Nicotine and the Developing Human". American Journal of Preventive Medicine. 49 (2): 286–93. doi:10.1016/j.amepre.2015.01.015. ISSN 0749-3797. PMC 4594223. PMID 25794473.
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  34. ↑ 34.00 34.01 34.02 34.03 34.04 34.05 34.06 34.07 34.08 34.09 34.10 34.11 34.12 34.13 34.14 34.15 34.16 34.17 34.18 34.19 34.20 34.21 Shehata, Shaimaa A.; Toraih, Eman A.; Ismail, Ezzat A.; Hagras, Abeer M.; Elmorsy, Ekramy; Fawzy, Manal S. (12 September 2023). "Vaping, Environmental Toxicants Exposure, and Lung Cancer Risk". Cancers. 15 (18): 4525. doi:10.3390/cancers15184525. PMC 10526315. PMID 37760496. {{cite journal}}: Check |pmc= value (help) This article incorporates text by Shaimaa A Shehata, Eman A Toraih, Ezzat A Ismail, Abeer M Hagras, Ekramy Elmorsy, and Manal S Fawzy available under the CC BY 4.0 license.
  35. ↑ 35.00 35.01 35.02 35.03 35.04 35.05 35.06 35.07 35.08 35.09 35.10 35.11 35.12 35.13 35.14 35.15 35.16 35.17 35.18 Schiliro, Marta; Vogel, Elizabeth R.; Paolini, Lucia; Pabelick, Christina M. (2021). "Cigarette Smoke Exposure, Pediatric Lung Disease, and COVID-19". Frontiers in Physiology. 12. doi:10.3389/fphys.2021.652198. ISSN 1664-042X. PMC 8110920. PMID 33986692. This article incorporates text by Marta Schiliro, Elizabeth R. Vogel, Lucia Paolini, and Christina M. Pabelick1 available under the CC BY 4.0 license.
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  45. ↑ Bolt, Alicia M.; Mann, Koren K. (December 2016). "Tungsten: an Emerging Toxicant, Alone or in Combination". Current Environmental Health Reports. 3 (4): 405–415. doi:10.1007/s40572-016-0106-z.
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  50. ↑ Bloom, Michael S.; Varde, Meghana; Newman, Roger B. (December 2022). "Environmental toxicants and placental function". Best Practice & Research Clinical Obstetrics & Gynaecology. 85: 105–120. doi:10.1016/j.bpobgyn.2022.09.003. PMID 36274037.
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  52. ↑ Wolff, Mary S.; Buckley, Jessie P.; Engel, Stephanie M.; McConnell, Rob S.; Barr, Dana B. (2017). "Emerging exposures of developmental toxicants". Current Opinion in Pediatrics. 29 (2): 218–224. doi:10.1097/MOP.0000000000000455. ISSN 1040-8703. PMC 5473289. PMID 28059904.
  53. ↑ 53.00 53.01 53.02 53.03 53.04 53.05 53.06 53.07 53.08 53.09 53.10 53.11 53.12 53.13 53.14 53.15 53.16 Dator, Romel P.; Solivio, Morwena J.; Villalta, Peter W.; Balbo, Silvia (4 June 2019). "Bioanalytical and Mass Spectrometric Methods for Aldehyde Profiling in Biological Fluids". Toxics. 7 (2): 32. doi:10.3390/toxics7020032. PMC 6630274. PMID 31167424. This article incorporates text by Romel P. Dator, Morwena. Solivio, Peter W. Villalta, and Silvia Balbo available under the CC BY 4.0 license.
  54. ↑ 54.0 54.1 54.2 54.3 54.4 54.5 54.6 Žuškin, Eugenija; Mustajbegović, Jadranka; Jelinić, Jagoda; Pucarin-Cvetković, Jasna; Milošević, Milan (1 December 2007). "Effects of Volcanic Eruptions on Environment and Health". Archives of Industrial Hygiene and Toxicology. 58 (4): 479–486. doi:10.2478/v10004-007-0041-3. PMID 18063533.} This article incorporates text by Eugenija Zuskin, Jadranka Mustajbegović, Jagoda Doko Jelinić, Jasna Pucarin-Cvetković, and Milan Milosević available under the CC BY 4.0 license.
  55. ↑ 55.0 55.1 55.2 Spence, Charles (19 November 2020). "Using Ambient Scent to Enhance Well-Being in the Multisensory Built Environment". Frontiers in Psychology. 11. doi:10.3389/fpsyg.2020.598859. PMC 7710513. PMID 33329267. This article incorporates text by Charles Spence available under the CC BY 4.0 license.
  56. ↑ Fazio, Emily (4 January 2024). "The Impact of Candles on Indoor Air Quality". Men's Journal.
  57. ↑ 57.00 57.01 57.02 57.03 57.04 57.05 57.06 57.07 57.08 57.09 57.10 57.11 57.12 "Air Pollution and the Brain". California Air Resources Board. 31 August 2018.Public Domain This article incorporates text from this source, which is in the public domain.
  58. ↑ "Particle Pollution". Centers for Disease Control and Prevention. 16 February 2023.Public Domain This article incorporates text from this source, which is in the public domain.
  59. ↑ 59.0 59.1 59.2 59.3 Qi, Ji; Zulfiker, Abu; Li, Chun; Good, David; Wei, Ming (20 August 2018). "The Development of Toad Toxins as Potential Therapeutic Agents". Toxins. 10 (8): 336. doi:10.3390/toxins10080336. This article incorporates text by Ji Qi, Abu Hasanat Md Zulfiker, Chun Li, David Good, and Ming Q. Wei available under the CC BY 4.0 license.
  60. ↑ Chan, Yau Sang; Cheung, Randy Chi Fai; Xia, Lixin; Wong, Jack Ho; Ng, Tzi Bun; Chan, Wai Yee (July 2016). "Snake venom toxins: toxicity and medicinal applications". Applied Microbiology and Biotechnology. 100 (14): 6165–6181. doi:10.1007/s00253-016-7610-9.
  61. ↑ Waheed, Humera; Moin, Syed F.; Choudhary, M. I. (4 July 2017). "Snake Venom: From Deadly Toxins to Life-saving Therapeutics". Current Medicinal Chemistry. 24 (17). doi:10.2174/0929867324666170605091546.
  62. ↑ Uzair, Bushra; Atlas, Nagina; Malik, Sidra Batool; Jamil, Nazia; Ojuolape, Salaam Temitope; Rehman, Mujaddad Ur; Khan, Barkat Ali (6 September 2018). "Snake Venom as an Effective Tool Against Colorectal Cancer". Protein & Peptide Letters. 25 (7): 626–632. doi:10.2174/0929866525666180614112935.
  63. ↑ 63.0 63.1 63.2 63.3 Goh, C. S. S.; Hodgson, D. R.; Fearnside, S. M.; Heller, J.; Malikides, N. (August 2005). "Sodium monofluoroacetate (Compound 1080) poisoning in dogs". Australian Veterinary Journal. 83 (8): 474–479. doi:10.1111/j.1751-0813.2005.tb13296.x.
  64. ↑ 64.0 64.1 64.2 64.3 64.4 Alshannaq, Ahmad; Yu, Jae-Hyuk (13 June 2017). "Occurrence, Toxicity, and Analysis of Major Mycotoxins in Food". International Journal of Environmental Research and Public Health. 14 (6): 632. doi:10.3390/ijerph14060632. PMC 5486318. PMID 28608841. This article incorporates text by Ahmad Alshannaq and Jae-Hyuk Yu available under the CC BY 4.0 license.
  65. ↑ 65.0 65.1 Linda Garverick (1 January 1994). Corrosion in the Petrochemical Industry. ASM International. pp. 103–. ISBN 978-0-87170-505-1.
  66. ↑ Pilotto, Louis S. (1995). "Disinfection of drinking water, disinfection by-products and cancer: what about Australia?". Australian Journal of Public Health. 19 (1): 89–93. doi:10.1111/j.1753-6405.1995.tb00304.x. ISSN 1035-7319. PMID 7734603.
  67. ↑ Rafael Vazquez-Duhalt; Rodolfo Quintero-Ramirez (18 September 2004). Petroleum Biotechnology: Developments and Perspectives. Elsevier. pp. 210–. ISBN 978-0-08-047371-0.
  68. ↑ Don Salm; Ron Sklansky (2001). Legislation on Recodification of Operating While Intoxicated and Safety Laws Pertaining to Motor Vehicle, All-terrain Vehicle, Boat Or Snowmobile Operation. Wisconsin Legislative Council. pp. 12–.
  69. ↑ Fahd Salem Bahammam (2013). Food and Dress in Islam: An explanation of matters relating to food and drink and dress in Islam. Modern Guide. pp. 1–. ISBN 978-1-909322-99-8.

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