News & Resources

Several cross-sectional studies of a single population of workers exposed to formaldehyde at one of two factories using or producing formaldehyde–melamine resins in China have concluded that formaldehyde exposure induces damage to hematopoietic cells that originate in the bone marrow.

Numerous contaminants in indoor air and their potential to cause or exacerbate asthma continue to be a subject of public health concern.

DNA-protein crosslinks (DPC) arise from a wide range of endogenous and exogenous chemicals, such as chemotherapeutic drugs and formaldehyde. Importantly, recent identification of aldehydes as endogenous genotoxins in Fanconi anemia has provided new insight into disease causation.

To determine whether the National Cancer Institute's (NCI) suggestion of a persistent increased mortality risk for nasopharyngeal cancer (NPC) in relation to formaldehyde (FA) exposure is robust with respect to alternative methods of data analysis.

In 2013, we proposed a novel bottom-up approach to bounding low-dose cancer risks that may result from small exogenous exposures to chemicals that are always present in the body as a result of normal biological processes.

To evaluate associations between cumulative and peak formaldehyde exposure and mortality from acute myeloid leukemia (AML) and other lymphohematopoietic malignancies.

Formaldehyde is not only a widely used chemical with well-known carcinogenicity but is also a normal metabolite of living cells.

A recently-completed study adds further compelling evidence that the current body of existing mode of action data do not support a causal association between formaldehyde and leukemia.

In 2004, the International Agency for Research on Cancer (IARC) reclassified formaldehyde (FA) from a probable (Group 2A) to a known human carcinogen (Group 1) citing results for nasopharyngeal cancer (NPC) mortality from the follow-up through 1994 of the National Cancer Institute formaldehyde cohort study.

MicroRNAs (miRNAs) are critical regulators of gene expression, yet much remains unknown regarding their changes resulting from environmental exposures as they influence cellular signaling across various tissues.

With formaldehyde as the major source of endogenous N⁶-formyllysine protein adducts, we quantified endogenous and exogenous N⁶-formyllysine in the nasal epithelium of rats exposed by inhalation to 0.7, 2, 5.8, and 9.1 ppm [¹³C²H₂]-formaldehyde using liquid chromatography-coupled tandem mass spectrometry.

Formaldehyde is an air pollutant present in both indoor and outdoor atmospheres. Because of its ubiquitous nature, it is imperative to understand the mechanisms underlying formaldehyde- induced toxicity and carcinogenicity. MicroRNAs (miRNAs) can influence disease caused by environmental exposures, yet miRNAs are understudied in relation to formaldehyde. Our previous investigation demonstrated that formaldehyde exposure in human lung cells caused disruptions in miRNA expression profiles in vitro.

Formaldehyde is a widely used high production chemical that is also released as a byproduct of combustion, off-gassing of various building products, and as a fixative for pathologists and embalmers.

We propose a novel bottom-up approach to the bounding of low-dose human cancer risks from chemical exposures that does not rely at all upon high-dose data for human or animal cancers.