The World Trade Center exposome and health effects in 9/11 rescue and recovery workers.

Background: In the aftermath of the World Trade Center (WTC) attack on 11 September 2001, rescue and recovery workers faced hazardous conditions and toxic agents. Prior research linked these exposures to adverse health effects, but mainly examined individual factors, overlooking complex mixture effects.

Methods: This study applies an exposomic approach encompassing the totality of responders' experience, defined as the WTC exposome.

Urinary biomarkers of environmental exposures and asthma morbidity in a school inner city asthma study.

Background: The burden of pediatric asthma and other allergic diseases is not evenly distributed among United States populations.

Objective: To determine whether urinary biomarkers are associated with asthma morbidity, and if associations vary by child race, ethnicity and sex.

Methods: This study includes n = 152 children with physician-diagnosed asthma who participated in the School Inner-City Asthma Intervention Study (SICAS-2).

Pulmonary osteoclast-like cells in silica induced pulmonary fibrosis.

The pathophysiology of silicosis is poorly understood, limiting development of therapies for those who have been exposed to the respirable particle. We explored mechanisms of silica-induced pulmonary fibrosis in human lung samples collected from patients with occupational exposure to silica and in a longitudinal mouse model of silicosis using multiple modalities including whole-lung single-cell RNA sequencing and histological, biochemical, and physiologic assessments. In addition to pulmonary inflammation and fibrosis, intratracheal silica challenge induced osteoclast-like differentiation of alveolar macrophages and recruited monocytes, driven by induction of the osteoclastogenic cytokine, receptor activator of nuclear factor κΒ ligand (RANKL) in pulmonary lymphocytes, and alveolar type II cells.

The effect of incidental ethanol exposures on the formation of blood phosphatidylethanol.

Blood phosphatidylethanol (PEth), a metabolite of ethanol, is emerging as a direct biomarker of choice for characterizing ethanol consumption in clinical, research, and forensic contexts. An accumulating body of evidence, and a recent international consensus conference, supports a cutoff of 20 μg/L of PEth (16:0/18:1) to distinguish abstinence from beverage ethanol consumption. There is a dearth of research, however, on whether exposures to nonbeverage ethanol sources are sufficient to produce PEth concentrations that exceed this cutoff.