Reproductive and developmental toxicity of formaldehyde: A systematic review

Abstract

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.

Adhesives based on formaldehyde – environmental problems

“…FA inhibits reproduction in both animals and humans, causing an increase in the incidence of menstrual disorders, inflammatory diseases of the reproductive tract, and sterility, and increased risk of spontaneous abortion and adverse developmental effects during pregnancy, such as low birth weights among offspring (Duong et al, 2011;TOXNET Database). It is categorized as a known human carcinogen by the International Agency for Research on Cancer (IARC).…”

Papel indicador colorimétrico para detecção de formol em produtos lácteos e produtos de higiene pessoal

“…Outros estudos também apontam que a exposição constante a formaldeído influencia de forma negativa o sistema hormonal e a reprodução humana. 4 Baseados nos estudos toxicológicos do formol, o órgão responsável pelo controle de produtos no Brasil, a ANVISA (Agência Nacional de Vigilância Sanitária), proibiu a comercialização do formol e restringiu sua utilização em alguns produtos cosméticos (Resolução-RDC nº 35, publicada em 3 de junho de 2008; e Resolução-RDC nº 36, publicada em 17 de junho de 2009). A proibição do formol e sua restrição também ocorrem em outros países, como, entre outros, os Estados Unidos, Inglaterra, Alemanha e Japão.…”

Formaldehyde-induced toxicity in the nasal epithelia of workers of a plastic laminate plant

“…1,6 FA related DNA-protein cross-links, chromosome mutations, sister-chromatid exchanges and micronuclei are considered relevant lesions, 7 but increased production of reactive oxygen species (ROS) and subsequent DNA damage and peroxidation of lipids play a relevant role in FA-induced toxicity. 8 FA causes genetic damage to the nasal tissues of both experimental animals and humans exposed by inhalation. 1 In particular, FA causes the production of malondialdehyde (MDA), or more correctly β-hydroxyacrolein, a reactive lipid peroxidation by-product.…”

“…1 In particular, FA causes the production of malondialdehyde (MDA), or more correctly β-hydroxyacrolein, a reactive lipid peroxidation by-product. 8 MDA is an aldehyde capable of interacting with DNA to form 3-(2-deoxy-β-D-erythropentafuranosyl)pyrimido[1,2-α]purin-10(3H)-one deoxyguanosine (M 1 dG) adducts. 9,10 Exocyclic M 1 dG adducts, if not repaired, may block cell replication and cause base pair and frameshift mutations in repeated sequences.…”