1 1157 130 CONTAMINANT METALS AS CARDIOVASCULAR RISK FACTORS: A SCIENTIFIC STATEMENT FROM THE AMERICAN HEART ASSOCIATION. EXPOSURE TO ENVIRONMENTAL POLLUTANTS IS LINKED TO INCREASED RISK OF CARDIOVASCULAR DISEASE. BEYOND THE EXTENSIVE EVIDENCE FOR PARTICULATE AIR POLLUTION, ACCUMULATING EVIDENCE SUPPORTS THAT EXPOSURE TO NONESSENTIAL METALS SUCH AS LEAD, CADMIUM, AND ARSENIC IS A SIGNIFICANT CONTRIBUTOR TO CARDIOVASCULAR DISEASE WORLDWIDE. HUMANS ARE EXPOSED TO METALS THROUGH AIR, WATER, SOIL, AND FOOD AND EXTENSIVE INDUSTRIAL AND PUBLIC USE. CONTAMINANT METALS INTERFERE WITH CRITICAL INTRACELLULAR REACTIONS AND FUNCTIONS LEADING TO OXIDATIVE STRESS AND CHRONIC INFLAMMATION THAT RESULT IN ENDOTHELIAL DYSFUNCTION, HYPERTENSION, EPIGENETIC DYSREGULATION, DYSLIPIDEMIA, AND CHANGES IN MYOCARDIAL EXCITATION AND CONTRACTILE FUNCTION. LEAD, CADMIUM, AND ARSENIC HAVE BEEN LINKED TO SUBCLINICAL ATHEROSCLEROSIS, CORONARY ARTERY STENOSIS, AND CALCIFICATION AS WELL AS TO INCREASED RISK OF ISCHEMIC HEART DISEASE AND STROKE, LEFT VENTRICULAR HYPERTROPHY AND HEART FAILURE, AND PERIPHERAL ARTERY DISEASE. EPIDEMIOLOGICAL STUDIES SHOW THAT EXPOSURE TO LEAD, CADMIUM, OR ARSENIC IS ASSOCIATED WITH CARDIOVASCULAR DEATH MOSTLY ATTRIBUTABLE TO ISCHEMIC HEART DISEASE. PUBLIC HEALTH MEASURES REDUCING METAL EXPOSURE ARE ASSOCIATED WITH REDUCTIONS IN CARDIOVASCULAR DISEASE DEATH. POPULATIONS OF COLOR AND LOW SOCIOECONOMIC MEANS ARE MORE COMMONLY EXPOSED TO METALS AND THEREFORE AT GREATER RISK OF METAL-INDUCED CARDIOVASCULAR DISEASE. TOGETHER WITH STRENGTHENING PUBLIC HEALTH MEASURES TO PREVENT METAL EXPOSURES, DEVELOPMENT OF MORE SENSITIVE AND SELECTIVE MEASUREMENT MODALITIES, CLINICAL MONITORING OF METAL EXPOSURES, AND THE DEVELOPMENT OF METAL CHELATION THERAPIES COULD FURTHER DIMINISH THE BURDEN OF CARDIOVASCULAR DISEASE ATTRIBUTABLE TO METAL EXPOSURE. 2023 2 5194 31 PRENATAL EXPOSURE TO POTENTIALLY TOXIC METALS AND THEIR EFFECTS ON GENETIC MATERIAL IN OFFSPRING: A SYSTEMATIC REVIEW. IN RECENT YEARS, THE BACKGROUND LEVEL OF ENVIRONMENTAL POLLUTANTS, INCLUDING METALS, HAS INCREASED. POLLUTANT EXPOSURE DURING THE EARLIEST STAGES OF LIFE MAY DETERMINE CHRONIC DISEASE SUSCEPTIBILITY IN ADULTHOOD BECAUSE OF GENETIC OR EPIGENETIC CHANGES. THE OBJECTIVE OF THIS REVIEW WAS TO IDENTIFY THE ASSOCIATION BETWEEN PRENATAL AND EARLY POSTNATAL EXPOSURE TO POTENTIALLY TOXIC METALS (PTMS) AND THEIR ADVERSE EFFECTS ON THE GENETIC MATERIAL OF OFFSPRING. A SYSTEMATIC REVIEW WAS CARRIED OUT FOLLOWING THE COCHRANE METHODOLOGY IN FOUR DATABASES: PUBMED, SCOPUS, WEB OF SCIENCE, AND THE COCHRANE LIBRARY. ELIGIBLE PAPERS WERE THOSE CONDUCTED IN HUMANS AND PUBLISHED IN ENGLISH BETWEEN 2010/01/01 AND 2021/04/30. A TOTAL OF 57 ARTICLES WERE INCLUDED, MOST OF WHICH EVALUATED PRENATAL EXPOSURE. MOST COMMONLY EVALUATED PTMS WERE AS, CD, AND PB. MAIN ADVERSE EFFECTS ON THE GENETIC MATERIAL OF NEWBORNS ASSOCIATED WITH PTM PRENATAL EXPOSURE WERE ALTERATIONS IN TELOMERE LENGTH, GENE OR PROTEIN EXPRESSION, MITOCHONDRIAL DNA CONTENT, METABOLOMICS, DNA DAMAGE, AND EPIGENETIC MODIFICATIONS. MANY OF THESE EFFECTS WERE SEX-SPECIFIC, BEING PREDOMINANT IN BOYS. ONE ARTICLE REPORTED A SYNERGISTIC INTERACTION BETWEEN AS AND HG, AND TWO ARTICLES OBSERVED ANTAGONISTIC INTERACTIONS BETWEEN PTMS AND ESSENTIAL METALS, SUCH AS CU, SE, AND ZN. THE FINDINGS IN THIS REVIEW HIGHLIGHT THAT THE PROBLEM OF PTM EXPOSURE PERSISTS, AFFECTING THE MOST SUSCEPTIBLE POPULATIONS, SUCH AS NEWBORNS. SOME OF THESE ASSOCIATIONS WERE OBSERVED AT LOW CONCENTRATIONS OF PTMS. MOST OF THE STUDIES HAVE FOCUSED ON SINGLE EXPOSURES; HOWEVER, THREE INTERACTIONS BETWEEN ESSENTIAL AND NONESSENTIAL METALS WERE OBSERVED, HIGHLIGHTING THAT METAL MIXTURES NEED MORE ATTENTION. 2023 3 363 36 AMBIENT AIR POLLUTION: HEALTH HAZARDS TO CHILDREN. AMBIENT AIR POLLUTION IS PRODUCED BY SOURCES INCLUDING VEHICULAR TRAFFIC, COAL-FIRED POWER PLANTS, HYDRAULIC FRACTURING, AGRICULTURAL PRODUCTION, AND FOREST FIRES. IT CONSISTS OF PRIMARY POLLUTANTS GENERATED BY COMBUSTION AND SECONDARY POLLUTANTS FORMED IN THE ATMOSPHERE FROM PRECURSOR GASES. AIR POLLUTION CAUSES AND EXACERBATES CLIMATE CHANGE, AND CLIMATE CHANGE WORSENS HEALTH EFFECTS OF AIR POLLUTION. INFANTS AND CHILDREN ARE UNIQUELY SENSITIVE TO AIR POLLUTION, BECAUSE THEIR ORGANS ARE DEVELOPING AND THEY HAVE HIGHER AIR PER BODY WEIGHT INTAKE. HEALTH EFFECTS LINKED TO AIR POLLUTION INCLUDE NOT ONLY EXACERBATIONS OF RESPIRATORY DISEASES BUT ALSO REDUCED LUNG FUNCTION DEVELOPMENT AND INCREASED ASTHMA INCIDENCE. ADDITIONAL OUTCOMES OF CONCERN INCLUDE PRETERM BIRTH, LOW BIRTH WEIGHT, NEURODEVELOPMENTAL DISORDERS, IQ LOSS, PEDIATRIC CANCERS, AND INCREASED RISKS FOR ADULT CHRONIC DISEASES. THESE EFFECTS ARE MEDIATED BY OXIDATIVE STRESS, CHRONIC INFLAMMATION, ENDOCRINE DISRUPTION, AND GENETIC AND EPIGENETIC MECHANISMS ACROSS THE LIFE SPAN. NATURAL EXPERIMENTS DEMONSTRATE THAT WITH INITIATIVES SUCH AS INCREASED USE OF PUBLIC TRANSPORTATION, BOTH AIR QUALITY AND COMMUNITY HEALTH IMPROVE. SIMILARLY, THE CLEAN AIR ACT HAS IMPROVED AIR QUALITY, ALTHOUGH EXPOSURE INEQUITIES PERSIST. OTHER EFFECTIVE STRATEGIES FOR REDUCING AIR POLLUTION INCLUDE ENDING RELIANCE ON COAL, OIL, AND GAS; REGULATING INDUSTRIAL EMISSIONS; REDUCING EXPOSURE WITH ATTENTION TO PROXIMITY OF RESIDENCES, SCHOOLS, AND CHILD CARE FACILITIES TO TRAFFIC; AND A GREATER AWARENESS OF THE AIR QUALITY INDEX. THIS POLICY REVIEWS BOTH SHORT- AND LONG-TERM HEALTH CONSEQUENCES OF AMBIENT AIR POLLUTION, ESPECIALLY IN RELATION TO DEVELOPMENTAL EXPOSURES. IT EXAMINES INDIVIDUAL, COMMUNITY, AND LEGISLATIVE STRATEGIES TO MITIGATE AIR POLLUTION. 2021 4 360 29 AMBIENT AIR POLLUTION AND BIOMARKERS OF HEALTH EFFECT. RECENTLY, THE AIR POLLUTION SITUATION OF OUR COUNTRY IS VERY SERIOUS ALONG WITH THE DEVELOPMENT OF URBANIZATION AND INDUSTRIALIZATION. STUDIES INDICATE THAT THE EXPOSURE OF AIR POLLUTION CAN CAUSE A RISE OF INCIDENCE AND MORTALITY OF MANY DISEASES, SUCH AS CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD), ASTHMA, MYOCARDIAL INFARCTION, AND SO ON. HOWEVER, THERE IS NOW GROWING EVIDENCE SHOWING THAT SIGNIFICANT AIR POLLUTION EXPOSURES ARE ASSOCIATED WITH EARLY BIOMARKERS IN VARIOUS SYSTEMS OF THE BODY. IN ORDER TO BETTER PREVENT AND CONTROL THE DAMAGE EFFECT OF AIR POLLUTION, THIS ARTICLE SUMMARIZES COMPREHENSIVELY EPIDEMIOLOGICAL STUDIES ABOUT THE BAD EFFECTS ON THE BIOMARKERS OF RESPIRATORY SYSTEM, CARDIOVASCULAR SYSTEM, AND GENETIC AND EPIGENETIC SYSTEM EXPOSURE TO AMBIENT AIR POLLUTION. 2017 5 5295 32 PROTECTIVE POTENTIAL OF THYMOQUINONE AGAINST CADMIUM, ARSENIC, AND LEAD TOXICITY: A SHORT REVIEW WITH EMPHASIS ON OXIDATIVE PATHWAYS. HEAVY METALS ARE AMONG THE MOST IMPORTANT ENVIRONMENTAL POLLUTIONS USED IN VARIOUS INDUSTRIES. THEIR EXTENSIVE USE HAS INCREASED HUMAN SUSCEPTIBILITY TO DIFFERENT CHRONIC DISEASES. TOXIC METAL EXPOSURE, ESPECIALLY CADMIUM, ARSENIC, AND LEAD, CAUSES OXIDATIVE DAMAGES, MITOCHONDRIAL DYSFUNCTION, AND GENETIC AND EPIGENETIC MODIFICATIONS. MEANWHILE, THYMOQUINONE (TQ) IS AN EFFECTIVE COMPONENT OF NIGELLA SATIVA OIL THAT PLAYS AN IMPORTANT ROLE IN PREVENTING THE DESTRUCTIVE EFFECTS OF HEAVY METALS. THE PRESENT REVIEW DISCUSSES HOW TQ CAN PROTECT VARIOUS TISSUES AGAINST OXIDATIVE DAMAGE OF HEAVY METALS. THIS REVIEW IS BASED ON THE RESEARCH REPORTED ABOUT THE PROTECTIVE EFFECTS OF TQ IN THE TOXICITY OF HEAVY METALS, APPROXIMATELY THE LAST 10 YEARS (2010-2021). SCIENTIFIC DATABASES, INCLUDING SCOPUS, WEB OF SCIENCE, AND PUBMED, WERE SEARCHED USING THE FOLLOWING KEYWORDS EITHER ALONE OR IN COMBINATION: CADMIUM, ARSENIC, LEAD, TQ, AND OXIDATIVE STRESS. TQ, AS A POTENT ANTIOXIDANT, CAN DISTRIBUTE TO CELLULAR COMPARTMENTS AND PREVENT OXIDATIVE DAMAGE OF TOXIC METALS. HOWEVER, DEPENDING ON THE TYPE OF TOXIC METAL AND THE CARRIER SYSTEM USED TO RELEASE TQ IN BIOLOGICAL SYSTEMS, ITS THERAPEUTIC DOSAGE RANGE MAY BE VARIED. 2023 6 4208 31 METAL CARCINOGEN EXPOSURE INDUCES CANCER STEM CELL-LIKE PROPERTY THROUGH EPIGENETIC REPROGRAMING: A NOVEL MECHANISM OF METAL CARCINOGENESIS. ARSENIC, CADMIUM, NICKEL AND HEXAVALENT CHROMIUM ARE AMONG THE MOST COMMON ENVIRONMENTAL POLLUTANTS AND POTENT CARCINOGENS. CHRONIC EXPOSURE TO THESE METALS CAUSES VARIOUS TYPES OF CANCER IN HUMANS, REPRESENTING A SIGNIFICANT ENVIRONMENTAL HEALTH ISSUE. ALTHOUGH UNDER ACTIVE INVESTIGATION, THE MECHANISMS OF METAL CARCINOGENESIS HAVE NOT BEEN CLEARLY DEFINED. ONE COMMON FEATURE OF THESE METAL CARCINOGENS IS THAT THEY ARE ALL ABLE TO CAUSE VARIOUS EPIGENETIC DYSREGULATIONS, WHICH ARE BELIEVED TO PLAY IMPORTANT ROLES IN THEIR CARCINOGENICITY. HOWEVER, HOW METAL CARCINOGEN-CAUSED EPIGENETIC DYSREGULATION CONTRIBUTES TO METAL CARCINOGENESIS REMAINS LARGELY UNKNOWN. THE EVOLUTION OF CANCER STEM CELL (CSC) THEORY HAS OPENED EXCITING NEW AVENUES FOR STUDYING THE MECHANISM OF METAL CARCINOGENESIS. INCREASING EVIDENCE INDICATES THAT CHRONIC METAL CARCINOGEN EXPOSURE PRODUCES CSC-LIKE CELLS THROUGH DYSREGULATED EPIGENETIC MECHANISMS. THIS REVIEW WILL FIRST PROVIDE SOME BRIEF INTRODUCTIONS ABOUT CSC, EPIGENETICS AND EPIGENETIC REGULATION OF CSCS; THEN SUMMARIZE PROGRESSES IN RECENT STUDIES ON METAL CARCINOGEN-INDUCED CSC-LIKE PROPERTY THROUGH EPIGENETIC REPROGRAMING AS A NOVEL MECHANISM OF METAL CARCINOGENESIS. SOME PERSPECTIVES FOR FUTURE STUDIES IN THIS FIELD ARE ALSO PRESENTED. 2019 7 1925 25 ENVIRONMENTAL EPIGENETICS IN METAL EXPOSURE. ALTHOUGH IT IS WIDELY ACCEPTED THAT CHRONIC EXPOSURE TO ARSENITE, NICKEL, CHROMIUM AND CADMIUM INCREASES CANCER INCIDENCE IN INDIVIDUALS, THE MOLECULAR MECHANISMS UNDERLYING THEIR ABILITY TO TRANSFORM CELLS REMAIN LARGELY UNKNOWN. CARCINOGENIC METALS ARE TYPICALLY WEAK MUTAGENS, SUGGESTING THAT GENETIC-BASED MECHANISMS MAY NOT BE PRIMARILY RESPONSIBLE FOR METAL-INDUCED CARCINOGENESIS. GROWING EVIDENCE SHOWS THAT ENVIRONMENTAL METAL EXPOSURE INVOLVES CHANGES IN EPIGENETIC MARKS, WHICH MAY LEAD TO A POSSIBLE LINK BETWEEN HERITABLE CHANGES IN GENE EXPRESSION AND DISEASE SUSCEPTIBILITY AND DEVELOPMENT. HERE, WE REVIEW RECENT ADVANCES IN THE UNDERSTANDING OF METAL EXPOSURE AFFECTING EPIGENETIC MARKS AND DISCUSS ESTABLISHMENT OF HERITABLE GENE EXPRESSION IN METAL-INDUCED CARCINOGENESIS. 2011 8 4881 40 OVERVIEW OF THE CARDIOVASCULAR EFFECTS OF ENVIRONMENTAL METALS: NEW PRECLINICAL AND CLINICAL INSIGHTS. ENVIRONMENTAL CAUSES OF CARDIOVASCULAR DISEASES (CVDS) ARE GLOBAL HEALTH ISSUES. IN PARTICULAR, AN ASSOCIATION BETWEEN METAL EXPOSURE AND CVDS HAS BECOME EVIDENT BUT CAUSAL EVIDENCE STILL LACKS. THEREFORE, THIS SYMPOSIUM AT THE SOCIETY OF TOXICOLOGY 2022 ANNUAL MEETING ADDRESSED EPIDEMIOLOGICAL, CLINICAL, PRE-CLINICAL ANIMAL MODEL-DERIVED AND MECHANISM-BASED EVIDENCE BY FIVE PRESENTATIONS: 1) AN EPIDEMIOLOGIC STUDY ON POTENTIAL CVD RISKS OF INDIVIDUALS EXPOSED OCCUPATIONALLY AND ENVIRONMENTALLY TO HEAVY METALS; 2) BOTH PRESENTATIONS OF THE SECOND AND THIRD WERE CLINICAL STUDIES FOCUSING ON THE POTENTIAL LINK BETWEEN HEAVY METALS AND PULMONARY ARTERIAL HYPERTENSION (PAH), BY PRESENTING ALTERED BLOOD METAL CONCENTRATIONS OF BOTH NON-ESSENTIAL AND ESSENTIAL METALS IN THE PATIENTS WITH PAH AND POTENTIAL THERAPEUTIC APPROACHES; 3) ARSENIC-INDUCED ATHEROSCLEROSIS VIA INFLAMMATORY CELLS IN MOUSE MODEL; 4) PATHOGENIC EFFECTS ON THE HEART BY ADULT CHRONIC EXPOSURE TO VERY LOW-DOSE CADMIUM VIA EPIGENETIC MECHANISMS AND WHOLE LIFE EXPOSURE TO LOW DOSE CADMIUM VIA EXACERBATING HIGH-FAT-DIET-LIPOTOXICITY. THIS SYMPOSIUM HAS BROUGHT EPIDEMIOLOGISTS, THERAPEUTIC INDUSTRY, PHYSICIANS, AND TRANSLATIONAL SCIENTISTS TOGETHER TO DISCUSS THE HEALTH RISKS OF OCCUPATIONAL AND ENVIRONMENTAL EXPOSURE TO HEAVY METALS THROUGH DIRECT CARDIOTOXICITY AND INDIRECT DISRUPTION OF HOMEOSTATIC MECHANISMS REGULATING ESSENTIAL METALS, AS WELL AS LIPID LEVELS. THE DATA SUMMARIZED BY THE PRESENTERS INFERS A POTENTIAL CAUSAL LINK BETWEEN MULTIPLE METALS AND CVDS AND DEFINES DIFFERENCES AND COMMONALITIES. THEREFORE, SUMMARY OF THESE PRESENTATIONS MAY ACCELERATE THE DEVELOPMENT OF EFFICIENT PREVENTIVE AND THERAPEUTIC STRATEGIES BY FACILITATING COLLABORATIONS AMONG MULTIDISCIPLINARY INVESTIGATORS. 2022 9 3566 33 IMPACT OF HEAVY METALS ON THE FEMALE REPRODUCTIVE SYSTEM. INTRODUCTION: IT HAS BEEN RECOGNIZED THAT ENVIRONMENTAL POLLUTION CAN AFFECT THE QUALITY OF HEALTH OF THE HUMAN POPULATION. HEAVY METALS ARE AMONG THE GROUP OF HIGHLY EMITTED CONTAMINANTS AND THEIR ADVERSE EFFECT OF LIVING ORGANISMS HAS BEEN WIDELY STUDIED IN RECENT DECADES. LIFESTYLE AND QUALITY OF THE AMBIENT ENVIRONMENT ARE AMONG THESE FACTORS WHICH CAN MAINLY CONTRIBUTE TO THE HEAVY METALS EXPOSURE IN HUMANS. OBJECTIVE: A REVIEW OF LITERATURE LINKING HEAVY METALS AND THE FEMALE REPRODUCTIVE SYSTEM AND DESCRIPTION OF THE POSSIBLE ASSOCIATIONS WITH EMISSION AND EXPOSURE OF HEAVY METALS AND IMPAIRMENTS OF FEMALE REPRODUCTIVE SYSTEM ACCORDING TO CURRENT KNOWLEDGE. RESULTS: THE POTENTIAL HEALTH DISORDERS CAUSED BY CHRONIC OR ACUTE HEAVY METALS TOXICITY INCLUDE IMMUNODEFICIENCY, OSTEOPOROSIS, NEURODEGENERATION AND ORGAN FAILURES. POTENTIAL LINKAGES OF HEAVY METALS CONCENTRATION FOUND IN DIFFERENT HUMAN ORGANS AND BLOOD WITH OESTROGEN-DEPENDENT DISEASES SUCH AS BREAST CANCER, ENDOMETRIAL CANCER, ENDOMETRIOSIS AND SPONTANEOUS ABORTIONS, AS WELL AS PRE-TERM DELIVERIES, STILLBIRTHS AND HYPOTROPHY, HAVE ALSO BEEN REPORTED. CONCLUSIONS: ENVIRONMENTAL DETERIORATION CAN LEAD TO THE ELEVATED RISK OF HUMAN EXPOSURE TO HEAVY METALS, AND CONSEQUENTLY, HEALTH IMPLICATIONS INCLUDING DISTURBANCES IN REPRODUCTION. IT IS THEREFORE IMPORTANT TO CONTINUE THE INVESTIGATIONS ON METAL-INDUCED MECHANISMS OF FERTILITY IMPAIRMENT ON THE GENETIC, EPIGENETIC AND BIOCHEMICAL LEVEL. 2015 10 300 32 AIR POLLUTION AND INDOOR SETTINGS. INDOOR ENVIRONMENTS CONTRIBUTE SIGNIFICANTLY TO TOTAL HUMAN EXPOSURE TO AIR POLLUTANTS, AS PEOPLE SPEND MOST OF THEIR TIME INDOORS. HOUSEHOLD AIR POLLUTION (HAP) RESULTING FROM COOKING WITH POLLUTING ("DIRTY") FUELS, WHICH INCLUDE COAL, KEROSENE, AND BIOMASS (WOOD, CHARCOAL, CROP RESIDUES, AND ANIMAL MANURE) IS A GLOBAL ENVIRONMENTAL HEALTH PROBLEM. INDOOR POLLUTANTS ARE GASES, PARTICULATES, TOXINS, AND MICROORGANISMS AMONG OTHERS, THAT CAN HAVE AN IMPACT ESPECIALLY ON THE HEALTH OF CHILDREN AND ADULTS THROUGH A COMBINATION OF DIFFERENT MECHANISMS ON OXIDATIVE STRESS AND GENE ACTIVATION, EPIGENETIC, CELLULAR, AND IMMUNOLOGICAL SYSTEMS. AIR POLLUTION IS A MAJOR RISK FACTOR AND CONTRIBUTOR TO MORBIDITY AND MORTALITY FROM MAJOR CHRONIC DISEASES. CHILDREN ARE SIGNIFICANTLY AFFECTED BY THE IMPACT OF THE ENVIRONMENT DUE TO BIOLOGICAL IMMATURITY, PRENATAL AND POSTNATAL LUNG DEVELOPMENT. POOR AIR QUALITY HAS BEEN RELATED TO AN INCREASED PREVALENCE OF CLINICAL MANIFESTATIONS OF ALLERGIC ASTHMA AND RHINITIS. HEALTH PROFESSIONALS SHOULD INCREASE THEIR ROLE IN MANAGING THE EXPOSURE OF CHILDREN AND ADULTS TO AIR POLLUTION WITH BETTER METHODS OF CARE, PREVENTION, AND COLLECTIVE ACTION. INTERVENTIONS TO REDUCE HOUSEHOLD POLLUTANTS MAY PROMOTE HEALTH AND CAN BE ACHIEVED WITH EDUCATION, COMMUNITY, AND HEALTH PROFESSIONAL INVOLVEMENT. 2021 11 1915 38 ENVIRONMENTAL AND OCCUPATIONAL EXPOSURE OF METALS AND FEMALE REPRODUCTIVE HEALTH. UNTAINTED ENVIRONMENT PROMOTES HEALTH, BUT THE LAST FEW DECADES EXPERIENCED STEEP UPSURGE IN ENVIRONMENTAL CONTAMINANTS POSING DETRIMENTAL PHYSIOLOGICAL IMPACT. THE RESPONSIBLE FACTORS MAINLY INCLUDE THE EXPONENTIAL GROWTH OF HUMAN POPULATION, HAVOC RISE IN INDUSTRIALIZATION, POORLY PLANNED URBANIZATION, AND SLAPDASH ENVIRONMENT MANAGEMENT. ENVIRONMENTAL DEGRADATION CAN INCREASE THE LIKELIHOOD OF HUMAN EXPOSURE TO HEAVY METALS, RESULTING IN HEALTH CONSEQUENCES SUCH AS REPRODUCTIVE PROBLEMS. AS A RESULT, RESEARCH INTO METAL-INDUCED CAUSES OF REPRODUCTIVE IMPAIRMENT AT THE GENETIC, EPIGENETIC, AND BIOCHEMICAL LEVELS MUST BE STRENGTHENED FURTHER. THESE METALS IMPACT UPON THE FEMALE REPRODUCTION AT ALL STRATA OF ITS REGULATION AND FUNCTIONS, BE IT DEVELOPMENT, MATURATION, OR ENDOCRINE FUNCTIONS, AND ARE LINKED TO AN INCREASE IN THE CAUSES OF INFERTILITY IN WOMEN. CHRONIC EXPOSURES TO THE HEAVY METALS MAY LEAD TO BREAST CANCER, ENDOMETRIOSIS, ENDOMETRIAL CANCER, MENSTRUAL DISORDERS, AND SPONTANEOUS ABORTIONS, AS WELL AS PRE-TERM DELIVERIES, STILLBIRTHS. FOR EXAMPLE, ENDOMETRIOSIS, ENDOMETRIAL CANCER, AND SPONTANEOUS ABORTIONS ARE ALL CAUSED BY THE METALLOESTROGEN CADMIUM (CD); LEAD (PB) LEVELS OVER A CERTAIN THRESHOLD CAN CAUSE SPONTANEOUS ABORTION AND HAVE A TERATOGENIC IMPACT; TOXIC AMOUNTS OF MERCURY (HG) HAVE AN INFLUENCE ON THE MENSTRUAL CYCLE, WHICH CAN LEAD TO INFERTILITY. IMPACT OF ENVIRONMENTAL EXPOSURE TO HEAVY METALS ON FEMALE FERTILITY IS THEREFORE A WELL-KNOWN FACT. THUS, THE UNDERLYING MECHANISMS MUST BE EXPLAINED AND PERIODICALLY UPDATED, GIVEN THE GROWING EVIDENCE ON THE INFLUENCE OF INCREASING ENVIRONMENTAL HEAVY METAL LOAD ON FEMALE FERTILITY. THE PURPOSE OF THIS REVIEW IS TO GIVE A CONCISE OVERVIEW OF HOW HEAVY METAL AFFECTS FEMALE REPRODUCTIVE HEALTH. 2022 12 1530 37 DNA METHYLATION CHANGES INDUCED BY PRENATAL TOXIC METAL EXPOSURE: AN OVERVIEW OF EPIDEMIOLOGICAL EVIDENCE. ACCUMULATING EVIDENCE SUGGESTS THAT EXPOSURE TO UNFAVORABLE CONDITIONS EARLY IN LIFE CAN SUBSTANTIALLY CONTRIBUTE TO THE RISK OF CHRONIC DISORDERS LATER IN LIFE ('DEVELOPMENTAL PROGRAMMING' PHENOMENON). THE MECHANISTIC BASIS FOR THIS PHENOMENON REMAINS POORLY UNDERSTOOD SO FAR, ALTHOUGH EPIGENETIC MECHANISMS SUCH AS DNA METHYLATION, HISTONE MODIFICATIONS AND MICRORNA-MEDIATED GENE REGULATION APPARENTLY PLAY A CRUCIAL ROLE. THE KEY ROLE OF EPIGENETIC MODIFICATIONS TRIGGERED BY UNFAVORABLE ENVIRONMENTAL CUES DURING SENSITIVE DEVELOPMENTAL PERIODS IN LINKING ADVERSE EARLY-LIFE EVENTS TO LATER-LIFE HEALTH OUTCOMES IS EVIDENT FROM A LARGE BODY OF STUDIES, INCLUDING METHYLOME-WIDE ASSOCIATION STUDIES AND RESEARCH OF CANDIDATE GENES. TOXIC METALS (TMS), SUCH AS HEAVY METALS, INCLUDING LEAD, CHROMIUM, CADMIUM, ARSENIC, MERCURY, ETC., ARE AMONG ENVIRONMENTAL CONTAMINANTS CURRENTLY MOST SIGNIFICANTLY IMPACTING HUMAN HEALTH STATUS. SINCE TMS CAN CROSS THE PLACENTAL BARRIER AND ACCUMULATE IN FETAL TISSUES, EXPOSURE TO HIGH DOSES OF THESE XENOBIOTICS EARLY IN DEVELOPMENT IS CONSIDERED TO BE AMONG IMPORTANT FACTORS CONTRIBUTING TO THE DEVELOPMENTAL PROGRAMMING OF ADULT-LIFE DISEASES IN MODERN SOCIETIES. IN THIS MINI-REVIEW, WE SUMMARIZE EPIDEMIOLOGICAL FINDINGS INDICATING THAT PRENATAL TM EXPOSURE CAN INDUCE EPIGENETIC DYSREGULATION, THEREBY POTENTIALLY AFFECTING ADULT HEALTH OUTCOMES. 2021 13 6313 31 THE RELATIONSHIP BETWEEN MERCURY EXPOSURE AND EPIGENETIC ALTERATIONS REGARDING HUMAN HEALTH, RISK ASSESSMENT AND DIAGNOSTIC STRATEGIES. BACKGROUND: EXPOSURE TO THE ENVIRONMENTAL TOXICANTS POSES A SERIOUS THREAT TO HUMAN HEALTH. THE EXTENT OF EXPOSURE AND THE DEVELOPMENT OF DISEASES ARE INTERRELATED WITH EACH OTHER. CHRONIC EXPOSURE TO MERCURY (HG) INCREASES THE RISK OF DEVELOPING SERIOUS HUMAN DISORDERS FROM EMBRYO TO ADULTHOOD. OBJECTIVES: THE PURPOSE OF THIS REVIEW IS TO HIGHLIGHT THE MOST COMMON HUMAN DISORDERS INDUCED BY HG EXPOSURE ON THE BASIS OF EPIGENETIC MECHANISMS. A GROWING BODY OF EVIDENCE SHOWS THAT HG EXPOSURE LEADS TO ALTERATIONS IN THE EPIGENETIC MARKERS. METHODS: WE PERFORMED AN ORGANIZED SEARCH OF THE AVAILABLE LITERATURE USING PUBMED, GOOGLE SCHOLAR, MEDLINE, REAXYS, EMBASE AND SCOPUS DATABASES. ALL THE RELEVANT CITATIONS, INCLUDING RESEARCH AND REVIEW ARTICLES IN ENGLISH WERE EVALUATED. THE SEARCH TERMS INCLUDED MERCURY, HG, EPIGENETICS, EPIGENETIC ALTERATIONS, DNA METHYLATION, HISTONE MODIFICATIONS, MICRORNAS (MIRNAS), AND RISK ASSESSMENT. RESULTS: DATA ON HUMAN TOXICITY DUE TO HG EXPOSURE SHOWS BROAD VARIATIONS IN TERMS OF CHEMICAL NATURE, DOSES, AND THE RATE OF EXPOSURE. HG CONSUMPTION EITHER VIA FOODS OR ENVIRONMENTAL SOURCES MAY CREATE DELETERIOUS HEALTH EFFECTS ON VARIOUS PHYSIOLOGICAL SYSTEMS AT LEAST PARTIALLY THROUGH AN EPIGENETIC MECHANISM. CONCLUSION: HG EXPOSURE COULD TRIGGER EPIGENETIC ALTERATIONS, HENCE LEADING TO VARIOUS HUMAN DISORDERS INCLUDING REDUCED NEWBORN CEREBELLUM SIZE, ADVERSE BEHAVIORAL OUTCOMES, ATHEROSCLEROSIS AND MYOCARDIAL INFARCTION. SIMILARLY, IN ADULTS, OCCUPATIONAL HG EXPOSURE HAS BEEN ASSOCIATED WITH AN INCREASED RISK OF AUTOIMMUNITY. IT HAS BEEN REVEALED THAT MIRNAS IN THE WOMAN'S CERVIX ARE A NOVEL RESPONDER TO MATERNAL HG EXPOSURE DURING PREGNANCY. HG-INDUCED EPIGENETIC ALTERATIONS ANALYSIS OF KIDNEY TISSUES SHOWED A SIGNIFICANT INTERRUPTION IN RENAL FUNCTION. DNA METHYLATION AND HISTONE POST-TRANSLATION MODIFICATIONS ARE PREDOMINANT TYPES OF HG EPIGENETIC ALTERATIONS. 2019 14 2605 30 EPIGENETICS-A POTENTIAL MEDIATOR BETWEEN AIR POLLUTION AND PRETERM BIRTH. PRETERM BIRTH IS A MAJOR CAUSE OF INFANT MORBIDITY AND MORTALITY AND A POTENTIAL RISK FACTOR FOR ADULT CHRONIC DISEASE. WITH OVER 15 MILLION INFANTS BORN PRETERM WORLDWIDE EACH YEAR, PRETERM BIRTH POSES A GLOBAL HEALTH CONCERN. THERE IS A POSSIBLE ASSOCIATION BETWEEN AIR POLLUTION AND PRETERM BIRTH, THOUGH STUDIES HAVE BEEN INCONSISTENT, LIKELY DUE TO VARIATION IN STUDY DESIGN. HOW AIR POLLUTION INDUCES HEALTH EFFECTS IS UNCERTAIN; HOWEVER, STUDIES HAVE REPEATEDLY DEMONSTRATED THE EFFECTS OF AIR POLLUTION ON EPIGENETIC MODIFICATIONS. MORE RECENT EVIDENCE SUGGESTS THAT EPIGENETICS MAY, IN TURN, BE LINKED TO PRETERM BIRTH. DISCOVERY OF ENVIRONMENTALLY MODIFIABLE EPIGENETIC PROCESSES CONNECTED TO PRETERM BIRTH MAY HELP TO IDENTIFY WOMEN AT RISK OF PRETERM BIRTH, AND ULTIMATELY LEAD TO DEVELOPMENT OF NEW PRETERM BIRTH PREVENTION MEASURES. 2016 15 1919 36 ENVIRONMENTAL ENDOCRINE DISRUPTORS: NEW DIABETOGENS? THE PREVALENCE OF TYPE-2 DIABETES HAS DRAMATICALLY INCREASED WORLDWIDE DURING THE LAST FEW DECADES. WHILE LIFESTYLE FACTORS (SEDENTARINESS, NOXIOUS FOOD), TOGETHER WITH GENETIC SUSCEPTIBILITY, ARE WELL-KNOWN ACTORS, THERE IS ACCUMULATING EVIDENCE SUGGESTING THAT ENDOCRINE DISRUPTING CHEMICALS (EDCS) MAY ALSO PLAY A PATHOPHYSIOLOGICAL ROLE IN THE OCCURRENCE OF METABOLIC DISEASES. BOTH EXPERIMENTAL AND EPIDEMIOLOGICAL EVIDENCE SUPPORT A ROLE FOR EARLY AND CHRONIC EXPOSURE TO LOW DOSES OF CHEMICAL POLLUTANTS WITH ENDOCRINE AND METABOLIC DISRUPTING EFFECTS. MOST ARE PRESENT IN THE FOOD CHAIN AND ACCUMULATE IN THE FAT MASS AFTER ABSORPTION. IN RODENTS, BISPHENOL A STIMULATES SYNTHESIS AND SECRETION OF PANCREATIC BETA CELLS AND DISTURBS INSULIN SIGNALING IN LIVER, MUSCLE AND ADIPOSE TISSUE THROUGH EPIGENETIC CHANGES LEADING TO INSULIN RESISTANCE AND BETA CELL IMPAIRMENT. IN HUMANS, EPIDEMIOLOGICAL REPORTS SHOW STATISTICAL LINK BETWEEN EXPOSURE TO PESTICIDES, POLYCHLORINATED BISPHENYLS, BISPHENOL A, PHTHALATES, DIOXINS OR AROMATIC POLYCYCLIC HYDROCARBIDES OR HEAVY METALS AND DT2 AFTER ACUTE ACCIDENTAL RELEASES OR EARLY IN LIFE AND/OR CHRONIC, LOW DOSES EXPOSURE. MORE PROSPECTIVE, LONGITUDINAL STUDIES ARE NEEDED TO DETERMINE THE IMPORTANCE OF SUCH ENVIRONMENTAL RISK FACTORS. 2017 16 1223 34 CRITICAL REVIEW ON EMERGING HEALTH EFFECTS ASSOCIATED WITH THE INDOOR AIR QUALITY AND ITS SUSTAINABLE MANAGEMENT. INDOOR AIR QUALITY (IAQ) IS ONE OF THE FUNDAMENTAL ELEMENTS AFFECTING PEOPLE'S HEALTH AND WELL-BEING. CURRENTLY, THERE IS A LACK OF AWARENESS AMONG PEOPLE ABOUT THE QUANTIFICATION, IDENTIFICATION, AND POSSIBLE HEALTH EFFECTS OF IAQ. AIRBORNE POLLUTANTS SUCH AS VOLATILE ORGANIC COMPOUNDS (VOCS), PARTICULATE MATTER (PM), SULFUR DIOXIDE (SO2), CARBON MONOXIDE (CO), NITROUS OXIDE (NO), POLYCYCLIC AROMATIC HYDROCARBONS (PAHS) MICROBIAL SPORES, POLLEN, ALLERGENS, ETC. PRIMARILY CONTRIBUTE TO IAQ DETERIORATION. THIS REVIEW DISCUSSES THE SOURCES OF MAJOR INDOOR AIR POLLUTANTS, MOLECULAR TOXICITY MECHANISMS, AND THEIR EFFECTS ON CARDIOVASCULAR, OCULAR, NEUROLOGICAL, WOMEN, AND FOETAL HEALTH. ADDITIONALLY, CONTEMPORARY STRATEGIES AND SUSTAINABLE METHODS FOR REGULATING AND REDUCING POLLUTANT CONCENTRATIONS ARE EMPHASIZED, AND CURRENT INITIATIVES TO ADDRESS AND ENHANCE IAQ ARE EXPLORED, ALONG WITH THEIR UNIQUE ADVANTAGES AND POTENTIALS. DUE TO THEIR LONGER EXPOSURE TIMES AND PARTICULAR PHYSICAL CHARACTERISTICS, WOMEN AND CHILDREN ARE MORE AT RISK FOR POOR INDOOR AIR QUALITY. BY TRIGGERING MANY TOXICITY MECHANISMS, INCLUDING OXIDATIVE STRESS, DNA METHYLATION, EPIGENETIC MODIFICATIONS, AND GENE ACTIVATION, INDOOR AIR POLLUTION CAN CAUSE A RANGE OF HEALTH ISSUES. LOW BIRTH WEIGHT, ACUTE LOWER RESPIRATORY TRACT INFECTIONS, SICK BUILDING SYNDROMES (SBS), AND EARLY DEATH ARE MORE PREVALENT IN EXPOSED RESIDENTS. ON THE OTHER HAND, THE MAIN CAUSES OF INCAPACITY AND EARLY MORTALITY ARE LUNG CANCER, CHRONIC OBSTRUCTIVE PULMONARY DISEASE, AND CARDIOVASCULAR DISORDERS. IT'S CRUCIAL TO ACKNOWLEDGE ANTICIPATED RESEARCH NEEDS AND IMPLEMENTED EFFICIENT INTERVENTIONS AND POLICIES TO LOWER HEALTH HAZARDS. 2023 17 1767 30 EARLY-LIFE EXPOSURE TO ENDOCRINE DISRUPTING CHEMICALS AND LATER-LIFE HEALTH OUTCOMES: AN EPIGENETIC BRIDGE? A GROWING BODY OF EVIDENCE DEMONSTRATES THAT ADVERSE EVENTS EARLY IN DEVELOPMENT, AND PARTICULARLY DURING INTRAUTERINE LIFE, MAY PROGRAM RISKS FOR DISEASES IN ADULT LIFE. INCREASING EVIDENCE HAS BEEN ACCUMULATED INDICATING THE IMPORTANT ROLE OF EPIGENETIC REGULATION INCLUDING DNA METHYLATION, HISTONE MODIFICATIONS AND MIRNAS IN DEVELOPMENTAL PROGRAMMING. AMONG THE ENVIRONMENTAL FACTORS WHICH PLAY AN IMPORTANT ROLE IN PROGRAMMING OF CHRONIC PATHOLOGIES, THE ENDOCRINE-DISRUPTING CHEMICALS (EDCS) THAT HAVE ESTROGENIC, ANTI-ESTROGENIC, AND ANTI-ANDROGENIC ACTIVITY ARE OF SPECIFIC CONCERN BECAUSE THE DEVELOPING ORGANISM IS EXTREMELY SENSITIVE TO PERTURBATION BY SUBSTANCES WITH HORMONE-LIKE ACTIVITY. AMONG EDCS, THERE ARE MANY SUBSTANCES THAT ARE CONSTANTLY PRESENT IN THE MODERN HUMAN ENVIRONMENT OR ARE IN WIDESPREAD USE, INCLUDING DIOXIN AND DIOXIN-LIKE COMPOUNDS, PHTHALATES, AGRICULTURAL PESTICIDES, POLYCHLORINATED BIPHENYLS, INDUSTRIAL SOLVENTS, PHARMACEUTICALS, AND HEAVY METALS. APART FROM THEIR COMMON ENDOCRINE ACTIVE PROPERTIES, SEVERAL EDCS HAVE BEEN SHOWN TO DISRUPT DEVELOPMENTAL EPIGENOMIC PROGRAMMING. THE PURPOSE OF THIS REVIEW IS TO PROVIDE A SUMMARY OF RECENT RESEARCH FINDINGS WHICH INDICATE THAT EXPOSURE TO EDCS DURING IN-UTERO AND/OR NEONATAL DEVELOPMENT CAN CAUSE LONG-TERM HEALTH OUTCOMES VIA MECHANISMS OF EPIGENETIC MEMORY. 2014 18 361 40 AMBIENT AIR POLLUTION AND THROMBOSIS. AIR POLLUTION IS A GROWING PUBLIC HEALTH CONCERN OF GLOBAL SIGNIFICANCE. ACUTE AND CHRONIC EXPOSURE IS KNOWN TO IMPAIR CARDIOVASCULAR FUNCTION, EXACERBATE DISEASE AND INCREASE CARDIOVASCULAR MORTALITY. SEVERAL PLAUSIBLE BIOLOGICAL MECHANISMS HAVE BEEN PROPOSED FOR THESE ASSOCIATIONS, HOWEVER, AT PRESENT, THE PATHWAYS ARE INCOMPLETE. A SEMINAL REVIEW BY THE AMERICAN HEART ASSOCIATION (2010) CONCLUDED THAT THE THROMBOTIC EFFECTS OF PARTICULATE AIR POLLUTION LIKELY CONTRIBUTED TO THEIR EFFECTS ON CARDIOVASCULAR MORTALITY AND MORBIDITY. THE AIM OF THE CURRENT REVIEW IS TO APPRAISE THE NEWLY ACCUMULATED SCIENTIFIC EVIDENCE (2009-2016) ON CONTRIBUTION OF HAEMOSTASIS AND THROMBOSIS TOWARDS CARDIOVASCULAR DISEASE INDUCED BY EXPOSURE TO BOTH PARTICULATE AND GASEOUS POLLUTANTS.SEVENTY FOUR PUBLICATIONS WERE REVIEWED IN-DEPTH. THE WEIGHT OF EVIDENCE SUGGESTS THAT ACUTE EXPOSURE TO FINE PARTICULATE MATTER (PM(2.5)) INDUCES A SHIFT IN THE HAEMOSTATIC BALANCE TOWARDS A PRO-THROMBOTIC/PRO-COAGULATIVE STATE. INSUFFICIENT DATA WAS AVAILABLE TO ASCERTAIN IF A SIMILAR RELATIONSHIP EXISTS FOR GASEOUS POLLUTANTS, AND VERY FEW STUDIES HAVE ADDRESSED LONG-TERM EXPOSURE TO AMBIENT AIR POLLUTION. PLATELET ACTIVATION, OXIDATIVE STRESS, INTERPLAY BETWEEN INTERLEUKIN-6 AND TISSUE FACTOR, ALL APPEAR TO BE POTENTIALLY IMPORTANT MECHANISMS IN POLLUTION-MEDIATED THROMBOSIS, TOGETHER WITH AN EMERGING ROLE FOR CIRCULATING MICROVESICLES AND EPIGENETIC CHANGES.OVERALL, THE RECENT LITERATURE SUPPORTS, AND ARGUABLY STRENGTHENS, THE CONTENTION THAT AIR POLLUTION CONTRIBUTES TO CARDIOVASCULAR MORBIDITY BY PROMOTING HAEMOSTASIS. THE VOLUME AND DIVERSITY OF THE EVIDENCE HIGHLIGHTS THE COMPLEXITY OF THE PATHOPHYSIOLOGIC MECHANISMS BY WHICH AIR POLLUTION PROMOTES THROMBOSIS; MULTIPLE PATHWAYS ARE PLAUSIBLE AND IT IS MOST LIKELY THEY ACT IN CONCERT. FUTURE RESEARCH SHOULD ADDRESS THE ROLE GASEOUS POLLUTANTS PLAY IN THE CARDIOVASCULAR EFFECTS OF AIR POLLUTION MIXTURE AND DIRECT COMPARISON OF POTENTIALLY SUSCEPTIBLE GROUPS TO HEALTHY INDIVIDUALS. 2018 19 2849 33 FROM AIR POLLUTION TO CARDIOVASCULAR DISEASES: THE EMERGING ROLE OF EPIGENETICS. THE ASSOCIATION BETWEEN AIR POLLUTION AND A WIDE-RANGING SPECTRUM OF ACUTE AND CHRONIC DISORDERS-INCLUDING CARDIOVASCULAR DISEASES-IS WIDELY ACKNOWLEDGED. EXPOSURE TO AIRBORNE POLLUTANTS TRIGGERS HARMFUL MECHANISMS SUCH AS OXIDATIVE STRESS AND SYSTEMIC INFLAMMATION, WHICH LEAD TO INCREASED INCIDENCE OF MYOCARDIAL INFARCTION, ARTERIAL HYPERTENSION, STROKE, AND HEART FAILURE. SUSTAINED EFFORTS HAVE BEEN MADE IN RECENT YEARS TO DISCOVER HOW ENVIRONMENTAL EXPOSURES AFFECT HUMAN HEALTH THROUGH EPIGENETIC PHENOMENA, SUCH AS DNA METHYLATION, HISTONE MODIFICATIONS AND NON-CODING RNA-MEDIATED GENE REGULATION. THIS REVIEW SUMMARIZES THE CURRENT EVIDENCES ON THE RELATIONSHIP BETWEEN AIR POLLUTION EXPOSURE, EPIGENETIC ALTERATIONS AND CARDIOVASCULAR IMPACT, IN VIEW OF PRESENT IMPLICATIONS AND FUTURE PERSPECTIVES. 2020 20 298 37 AIR POLLUTION AND AIRWAY DISEASE. EPIDEMIOLOGICAL AND TOXICOLOGICAL RESEARCH CONTINUES TO SUPPORT A LINK BETWEEN URBAN AIR POLLUTION AND AN INCREASED INCIDENCE AND/OR SEVERITY OF AIRWAY DISEASE. DETRIMENTAL EFFECTS OF OZONE (O(3)), NITROGEN DIOXIDE (NO(2)) AND PARTICULATE MATTER (PM), AS WELL AS TRAFFIC-RELATED POLLUTION AS A WHOLE, ON RESPIRATORY SYMPTOMS AND FUNCTION ARE WELL DOCUMENTED. NOT ONLY DO WE HAVE STRONG EPIDEMIOLOGICAL EVIDENCE OF A RELATIONSHIP BETWEEN AIR POLLUTION AND EXACERBATION OF ASTHMA AND RESPIRATORY MORBIDITY AND MORTALITY IN PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD), BUT RECENT STUDIES, PARTICULARLY IN URBAN AREAS, HAVE SUGGESTED A ROLE FOR POLLUTANTS IN THE DEVELOPMENT OF BOTH ASTHMA AND COPD. SIMILARLY, WHILE PREVALENCE AND SEVERITY OF ATOPIC CONDITIONS APPEAR TO BE MORE COMMON IN URBAN COMPARED WITH RURAL COMMUNITIES, EVIDENCE IS EMERGING THAT TRAFFIC-RELATED POLLUTANTS MAY CONTRIBUTE TO THE DEVELOPMENT OF ALLERGY. FURTHERMORE, NUMEROUS EPIDEMIOLOGICAL AND EXPERIMENTAL STUDIES SUGGEST AN ASSOCIATION BETWEEN EXPOSURE TO NO(2) , O(3) , PM AND COMBUSTION PRODUCTS OF BIOMASS FUELS AND AN INCREASED SUSCEPTIBILITY TO AND MORBIDITY FROM RESPIRATORY INFECTION. GIVEN THE CONSIDERABLE CONTRIBUTION THAT TRAFFIC EMISSIONS MAKE TO URBAN AIR POLLUTION RESEARCHERS HAVE SOUGHT TO CHARACTERIZE THE RELATIVE TOXICITY OF TRAFFIC-RELATED PM POLLUTANTS. RECENT ADVANCES IN MECHANISMS IMPLICATED IN THE ASSOCIATION OF AIR POLLUTANTS AND AIRWAY DISEASE INCLUDE EPIGENETIC ALTERATION OF GENES BY COMBUSTION-RELATED POLLUTANTS AND HOW POLYMORPHISMS IN GENES INVOLVED IN ANTIOXIDANT PATHWAYS AND AIRWAY INFLAMMATION CAN MODIFY RESPONSES TO AIR POLLUTION EXPOSURES. OTHER INTERESTING EPIDEMIOLOGICAL OBSERVATIONS RELATED TO INCREASED HOST SUSCEPTIBILITY INCLUDE A POSSIBLE LINK BETWEEN CHRONIC PM EXPOSURE DURING CHILDHOOD AND VULNERABILITY TO COPD IN ADULTHOOD, AND THAT INFANTS SUBJECTED TO HIGHER PRENATAL LEVELS OF AIR POLLUTION MAY BE AT GREATER RISK OF DEVELOPING RESPIRATORY CONDITIONS. WHILE THE CHARACTERIZATION OF POLLUTANT COMPONENTS AND SOURCES PROMISE TO GUIDE POLLUTION CONTROL STRATEGIES, THE IDENTIFICATION OF SUSCEPTIBLE SUBPOPULATIONS WILL BE NECESSARY IF TARGETED THERAPY/PREVENTION OF POLLUTION-INDUCED RESPIRATORY DISEASES IS TO BE DEVELOPED. 2011