Documents teratogenic effects 17 results

"Objectives
This prospective birth cohort study evaluated the effect of occupational exposure to endocrine disrupting chemicals (EDC) during pregnancy on inadequate fetal growth as measured by small-for-gestational age (SGA) and inadequate fetal growth measured by percentage of optimal birth weight (POBW). The study also identified the maternal characteristics associated with an increased risk of exposure to EDC.
Methods
We studied 4142 pregnant women who were in paid employment during pregnancy and participated in a population-based, prospective 2007–2011 birth cohort study, the Born in Bradford Study, with an estimated participation of 80%. Job titles were coded at 26–28 weeks` gestation at a 4-digit level according to 353 unit groups in the 2000 UK Standard Occupational Classification. They were then linked to expert judgment on exposure to each of ten EDC groups as assessed through a job exposure matrix (JEM). We performed generalized estimation equation modelling by a modified Poisson regression to assess the risk of POBW and SGA associated with an increased risk of chemical exposures.
Results
The frequency of POBW<85 significantly increased for mothers exposed to pesticides [adjusted risk ratio (RRadj) 3.72, 95% confidence interval (CI) 1.40–9.91] and phthalates (RRadj 3.71, 95% CI 1.62–8.51). There was a 5-fold increase risk of SGA for mothers exposed to pesticides (RRadj 5.45, 95% CI 1.59–18.62). Veterinary nurses and horticultural trades were most frequently associated with exposure to pesticides while hairdressers, beauticians, and printing machine minders were associated with phthalates.
Conclusion
Maternal occupational exposure to estimated concentrations of pesticides and phthalates is associated with impaired fetal growth.

"Ochratoxin A (OTA) is nephrotoxic, hepatotoxic, reprotoxic, embryotoxic, teratogenic, neurotoxic, immunotoxic, and carcinogenic for laboratory and farm animals. Male and female reproductive health has deteriorated in many countries during the last few decades. A number of toxins in environment are suspected to affect reproductive system in male and female. OTA is one of them. OTA has been found to be teratogenic in several animal models including rat, mouse, hamster, quail, and chick, with reduced birth weight and craniofacial abnormalities being the most common signs. The presence of OTA also results in congenital defects in the fetus. Neither the potential of OTA to cause malformations in human nor its teratogenic mode of action is known. Exposure to OTA leads to increased embryo lethality manifested as resorptions or dead fetuses. The mechanism of OTA transfer across human placenta (e.g., which transporters are involved in the transfer mechanism) is not fully understood. Some of the toxic effects of OTA are potentiated by other mycotoxins or other contaminants. Therefore, OTA exposure of pregnant women should be minimized. OTA has been shown to be an endocrine disruptor and a reproductive toxicant, with abilities of altering sperm quality. Other studies have shown that OTA is a testicular toxin in animals. Thus, OTA is a biologically plausible cause of testicular cancer in man."

"Le bisphénol A (BPA), substance de synthèse intervenant dans la composition de nombreux objets, est soupçonné de perturber le fonctionnement hormonal. Des études récentes semblent mettre en évidence des effets sur la santé à faibles doses mais ne font pas consensus. L'Anses apporte de nouveaux éléments en montrant qu'il existe des risques présumés pour le développement du foetus suite à l'exposition au BPA des femmes enceintes exerçant le métier de caissière."

"Exposure to pesticides is a known risk for human health. This paper describes the relationship between parental exposure and congenital malformations in the newborn. Objective: To study the association between exposure to pesticides and congenital malformations in neonates born in the Regional Hospital of Encarnacion, in the Department of Itapua, Paraguay. Materials and Methods: A prospective casecontrolled study carried out from March 2006 to February 2007. Cases included all newborns with congenital malformations, and controls were all healthy children of the same sex born immediately thereafter. Births outside the hospital were not counted. Exposure was considered to be any contact with agricultural chemicals, in addition to other known risk factors for congenital defects. Results: A total of 52 cases and 87 controls were analyzed. The average number of births each month was 216. The significantly associated risk factors were: living near treated fields (OR 2.46, CI 95% 1.095.57, p<0.02), dwelling located less than 1 Km. (OR 2.66, CI 95%; 1.195.97, p<0.008), storage of pesticides in the home (OR 15.35, CI 95%, 1.96701.63), p<0.03), direct or accidental contact with pesticides (OR 3.19, CI 95%, 0.9711.4, p<0.04), and family history of malformation (OR 6.81, CI 5%, 1.9430.56, p<0.001). Other known risk factors for malformations did not show statistical significance. Conclusion:
The results show an association between exposure to pesticides and congenital malformations. Further studies are required to confirm these findings. Key words: congenital malformations, agricultural chemicals, pesticide exposure."

""I died in Vietnam, but I didn't even know it," said a young Vietnam vet on the Today Show one morning in 1978, shocking viewers across the country. Waiting for an Army to Die: The Tragedy of Agent Orange—the first book ever written on the effects of Agent Orange—tells this young vet's story and that of hundreds of thousands of other former American servicemen. During the war, the US sprayed an estimated 12 million gallons of Agent Orange on Vietnam, in order to defoliate close to 5 million acres of its land. "Had anyone predicted that millions of human beings exposed to Agent Orange/dioxin would get sick and die," scholar Fred A. Wilcox writes in the new introduction to his seminal book, "their warnings would have been dismissed as sci-fi fantasy or apocalyptic nonsense. Told in a gripping and compassionate narrative style that travels from the war in Vietnam to the war at home, and through portraits of many of the affected survivors, their families, and the doctors and scientists whose clinical experience and research gave the lie to the government whitewash, Waiting for an Army to Die tells a story that, thirty years later, continues to create new twists and turns for Americans still waiting for justice and an honest account of what happened to them.
Vietnam has chosen August 10—the day that the US began spraying Agent Orange on Vietnam—as Agent Orange Day, to commemorate all its citizens who were affected by the deadly chemical. The new second edition of Waiting for an Army to Die will be released upon the third anniversary of this day, in honor of all those whose families have suffered, and continue to suffer, from this tragedy."

"…a book about the health and environmental threats created by man-made chemical contaminants that intefere with hormones in humans and wildlife. endocrine disrupting chemicals alter development of the fetus in the womb by interfering with the natural hormonal signals directing fetal growth. their impacts, sometimes not detectable until years or decades after exposure, include reduced disease resistance, diminished fertility and compromised intelligence and behavior. our stolen future tells the story of how endocrine disruption was discovered, how it works what it means, and how families can protect themselves and their communities, all in clear, simple language intended for a general audience...", from foreword by vice president Al Gore.

"Formaldehyde, the recently classified carcinogen and ubiquitous environmental contaminant, has long been suspected of causing adverse reproductive and developmental effects, but previous reviews were inconclusive, due in part, to limitations in the design of many of the human population studies. In the current review, we systematically evaluated evidence of an association between formaldehyde exposure and adverse reproductive and developmental effects, in human populations and in vivo animal studies, in the peer-reviewed literature. The mostly retrospective human studies provided evidence of an association of maternal exposure with adverse reproductive and developmental effects. Further assessment of this association by meta-analysis revealed an increased risk of spontaneous abortion (1.76, 95% CI 1.20-2.59, p=0.002) and of all adverse pregnancy outcomes combined (1.54, 95% CI 1.27-1.88, p<0.001), in formaldehyde-exposed women, although differential recall, selection bias, or confounding cannot be ruled out. Evaluation of the animal studies including all routes of exposure, doses and dosing regimens studied, suggested positive associations between formaldehyde exposure and reproductive toxicity, mostly in males. Potential mechanisms underlying formaldehyde-induced reproductive and developmental toxicities, including chromosome and DNA damage (genotoxicity), oxidative stress, altered level and/or function of enzymes, hormones and proteins, apoptosis, toxicogenomic and epigenomic effects (such as DNA methylation), were identified. To clarify these associations, well-designed molecular epidemiologic studies, that include quantitative exposure assessment and diminish confounding factors, should examine both reproductive and developmental outcomes associated with exposure in males and females. Together with mechanistic and animal studies, this will allow us to better understand the systemic effect of formaldehyde exposure."