To better understand the science linking environmental contaminants exposures with adverse pregnancy outcomes, we reviewed the relevant epidemiologic literature. We searched PubMed (primarily 1995-2006) using the key word combinations for select environmental exposures and pregnancy outcomes. Environmental tobacco smoke is a risk factor for reduced birth weight and preterm delivery. Outdoor air pollution is associated with reduced term birth weight and preterm delivery. Suggestive evidence associates pesticides and polychlorinated biphenyls with decreased fetal growth and length of gestation. Stronger evidence, primarily occupational, links certain birth defects with exposure to organic solvents and chlorophenoxy herbicides. Evidence suggests dichlorodiphenyltrichloroethane and bisphenol-A could be associated with pregnancy loss. Exposures in utero can also increase the risk of developmental delays (ie, impaired neurological function), adult chronic illnesses (ie, heart disease, diabetes, cancer), and next generation effects (ie, reduced reproductive capacity). Further research, education, and improved public health policy are needed to reduce potentially adverse exposures.

Environmental Exposures and Adverse Pregnancy Outcomes: A Review of the Science

DDT, DDE, and DDD ii DISCLAIMER The use of company or product name(s) is for identification only and does not imply endorsement by the Agency for Toxic Substances and Disease Registry. Toxicological profiles are revised and republished as necessary, but no less than once every three years. For information regarding the update status of previously released profiles, contact ATSDR at: V FOmWORD This toxicological profile is prepared in accordance with guidelines* developed by the Agency for Toxic Substances and Disease Registry (ATSDR) and the Environmental Protection Agency (EPA). The original guidelines were published in the Federal Register on April 17, 1987. Each profile will be revised and republished as necessary. The ATSDR toxicological profile succinctly characterizes the toxicologic and adverse health effects information for the hazardous substance described therein. Each peer-reviewed profile identifies and reviews the key literature that describes a hazardous substance's toxicologic properties. Other pertinent literature is also presented, but is described in less detail than the key studies. The profile is not intended to be an exhaustive document; however, more comprehensive sources of specialty information are referenced. The focus of the profiles is on health and toxicologic information; therefore, each toxicological profile begins with a public health statement that describes, in nontechnical language, a substance's reIevant toxicological properties. Following the public health statement is information concerning levels of si,gnificant human exposure and, where known, significant health effects. The adequacy of information to determine a substance's health effects is described in a health effects summary. Data needs that are of significance to protection of public health are identified by ATSDR and EPA. Each profile includes the following: The examination, summary, and interpretation of available toxicologic information and epidemiologic evaluations on a hazardous substance to ascertain the levels of significant human exposure for the substance and the associated acute, subacute, and chronic health effects; A determination of whether adequate information on the health effects of each substance is available or in the process of development to determine levels of exposure that present a significant risk to human health of acute, subacute, and chronic health effects; and Where appropriate, identification of toxicologic testing needed to identify the types or levels of exposure that may present significant risk of adverse health effects in humans. principal audiences for the toxicological profiles are health professionals at the federal, state, and local levels; interested private sector organizations and groups; and members of the public. …

/pdf/toxicological-profile-for-ddt-dde-and-ddd-2zxtxz16v4.pdf

Toxicological profile for DDT, DDE, and DDD

BACKGROUND Cigarette smoking is associated with lower fecundity rates, adverse reproductive outcomes and a higher risk of IVF failures. Over the last few decades, prevalence of smoking among women of reproductive age has increased. This review focuses on current knowledge of the potential effects of smoke toxicants on all reproductive stages and the consequences of smoke exposure on reproductive functions. METHODS We conducted a systematic review of the scientific literature on the impact of cigarette smoking and smoke constituents on the different stages of reproductive function, including epidemiological, clinical and experimental studies. We attempted to create hypotheses and find explanations for the deleterious effects of cigarette smoke observed in experimental studies. RESULTS Cigarette smoke contains several thousand components (e.g. nicotine, polycyclic aromatic hydrocarbons and cadmium) with diverse effects. Each stage of reproductive function, folliculogenesis, steroidogenesis, embryo transport, endometrial receptivity, endometrial angiogenesis, uterine blood flow and uterine myometrium is a target for cigarette smoke components. The effects of cigarette smoke are dose-dependent and are influenced by the presence of other toxic substances and hormonal status. Individual sensitivity, dose, time and type of exposure also play a role in the impact of smoke constituents on human fertility. CONCLUSIONS All stages of reproductive functions are targets of cigarette smoke toxicants. Further studies are necessary to better understand the deleterious effects of cigarette smoke compounds on the reproductive system in order to improve health care, help to reduce cigarette smoking and provide a better knowledge of the molecular mechanisms involved in reproductive toxicology.

/pdf/effects-of-cigarette-smoking-on-reproduction-vm5jxhs88u.pdf

Effects of cigarette smoking on reproduction

During therapeutic trials with E. coli L-asparaginase in 131 children and 143 adults with neoplastic disease the following signs of toxicity have been observed: fever, nausea and vomiting, weight loss, somnolence, lethargy, confusion, hypolipidemia, hyperlipidemia, hypoproteinemia, abnormal liver function tests, fatty metamorphosis of the liver, pancreatitis (in rare instances), azotemia, granulocytopenia, lymphopenia, thrombocytopenia, and hypersensitivity reactions. While these effects have been moderately severe and reversible in most instances, some patients have shown dangerous degrees of toxicity. This has been the case most frequently in adult patients receiving a dose of 5000 IU/kg/day.

https://acsjournals.onlinelibrary.wiley.com/doi/pdf/10.1002/1097-0142%28197002%2925%3A2%3C253%3A%3AAID-CNCR2820250204%3E3.0.CO%3B2-U

Toxicity of E. coli L-asparaginase in man.

We conducted an epidemiologic study to test the hypothesis that women who smoke have reduced fertility. Data on smoking history and number of noncontracepting cycles until conception were collected from 678 pregnant women. Thirty-eight percent of nonsmokers conceived in their first cycle compared with 28% of smokers. Smokers were 3.4 times more likely to have taken greater than a year to conceive compared with nonsmokers. After adjusting for potential confounding variables by Cox proportional hazards regression, fertility of smokers was estimated to be 72% of the fertility of nonsmokers. Heavy smokers experienced lower fertility than did light smokers (57% and 75% of the pregnancy rate of nonsmokers, respectively). Fertility was not affected by the husband's smoking. These data provide evidence that reduced fertility should be added to the growing list of reproductive hazards of cigarette smoking. ( JAMA 1985;253:2979-2983)

https://jamanetwork.com/journals/jama/articlepdf/398676/jama_253_20_031.pdf

Cigarette Smoking Associated With Delayed Conception

CAFFEINE and nicotine are examples of compounds from our chemical environment to which we are widely and constantly exposed and for which there are some indications of toxic effects on various aspects of reproduction. Caffeine effects chromosomal breakages in both plants and animals1, and an increased incidence of congenital malformations in the offspring of mice treated with this compound has been observed2. Caffeine also possesses mutagenic properties, although it has been estimated that this risk for humans is small3.

Caffeine and Nicotine penetrate the Pre-implantation Blastocyst

Embryotoxic effect of poly I. poly C.

1 After administration of p, p'-DDT to pregnant rabbits DDT and its metabolites are found in high concn in both the foetus and the organs of the maternal rabbit which regulate the foetal environment2 pp''-DDT does not rapidly leave the foetal tissue, as whole body levels at day 26 (17 days after DDT dosing) are higher than those in foetal plasma; foetal whole body levels are also higher than those found in placenta or maternal plasma, and half of those of maternal liver3 pp'-DDT treatment of pregnant rabbits at doses of 10 and 50 mg/kg caused an increased incidence of prematurity, an increase in the number of foetal resorptions and a decrease in foetal weight4 These doses of DDT did not increase the incidence of chromosomal aberrations in the maternal or foetal tissue and exposure in vitro to levels as high as 100 μg/ml caused no abnormalities

Distribution and Effects of DDT in the Pregnant Rabbit

L-Asparaginase catalyses the hydrolysis of L-asparagine to L-aspartic acid and ammonia. Interest in this enzyme has been stimulated by the discovery that it inhibits the growth of several experimental tumours1–3. L-Asparaginase is being used clinically to treat various leukaemias, lymphomas arid melanomas4, and it was recently shown to inhibit the early mitosis of regenerating livers in rats5. This communication concerns the effects of L-asparaginase on another rapidly growing tissue, the rabbit embryo.

Embryotoxic effect of L-asparaginase.

Accumulation of Nicotine in the Uterine Fluid of the Six-Day Pregnant Rabbit*

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