Rationale: Although short-term exposure to air pollution has been associated with acute, reversible lung function decrements, the impact of long-term exposure has not been well established. Objectives: To evaluate the association between long-term exposure to ozone (O3), particulate matter less than 10 μm in diameter (PM10), and nitrogen dioxide (NO2) and lung function growth in Mexico City schoolchildren. Methods: A dynamic cohort of 3,170 children aged 8 years at baseline was followed from April 23, 1996, through May 19, 1999. The children attended 39 randomly selected elementary schools located near 10 air quality monitoring stations and were visited every 6 months. Statistical analyses were performed using general linear mixed models. Measurements and Main Results: After adjusting for acute exposure and other potential confounding factors, deficits in FVC and FEV1 growth over the 3-year follow-up period were significantly associated with exposure to O3, PM10, and NO2. In multipollutant models, an interquartile range (IQR) increase in mean O3 concentration (IQR, 11.3 ppb) was associated with an annual deficit in FEV1 of 12 ml in girls and 4 ml in boys, an IQR range (IQR, 36.4 μg/m3) increase in PM10 with an annual deficit in FEV1 of 11 ml in girls and 15 ml in boys, and an IQR range (IQR, 12.0 ppb) increase in NO2 with an annual deficit in FEV1 of 30 ml in girls and 25 ml in boys. Conclusions: We conclude that long-term exposure to O3, PM10, and NO2 is associated with a deficit in FVC and FEV1 growth among schoolchildren living in Mexico City.

Environmental Health Perspectives is an Open Access journal published by the National Institute of Environmental Health Sciences. Environmental Health Perspectives is an Open Access journal published by the National Institute of Environmental Health Sciences.

Lead (Pb) has been used by humans since prehistoric times to make tools due to its malleability and durability. The Roman Empire, the Industrial Revolution, and the introduction of Pb in gasoline during the 1920s contributed to increased environmental concentrations. Pb toxicity led to its removal from gasoline after several decades. However, Pb continues to be emitted from various anthropogenic sources, including but not limited to batteries, mining, foundries, smelting, e-waste recycling, and painting. Pb remains an environmental concern, as no established safe concentration for human health has been identified. Children are more susceptible to the absorption and poisoning of Pb. Occupational exposure to Pb poses a significant risk to workers and individuals living near lead industries. The primary routes of exposure are inhalation and ingestion, and bioaccumulation and biomagnification through the food chain are major sources of human exposure. This review aims to provide an overview of Pb and its systemic toxicity of Pb, including its effects on the lungs, blood, liver, kidneys, and nervous, cardiovascular, and reproductive systems. Since Pb is classified as a probable carcinogen for humans, the article also addresses genotoxicity and cancer risk. Furthermore, it reviews the most researched mechanisms of toxicity, including calcium mimicry, oxidative stress, and inflammation, along with other less-studied mechanisms. Nevertheless, the authors emphasize the importance of exploring less examined cells, tissues, and mechanisms to deepen the understanding of Pb toxicity at various concentrations, particularly in cases of chronic low-level Pb exposure, to develop better prevention and treatment strategies for lead poisoning.

Altered claudin expression is related to metastatic potential, poor prognosis, or tumor recurrence. We analyzed if the overexpression of claudin-6, claudin-7, or claudin-9 in AGS cells altered cell motility, invasiveness, or proliferation rate. Claudin-7, claudin-9, and claudin-6 enhanced their invasive potential by 3.4-fold, 1.6-fold, and 2.0-fold, respectively. Claudin-6 and claudin-9 enhanced cell migration, while the proliferation rate of claudin-6-, claudin-7-, and claudin-9-transfected cells increased by 12.7%, 9.0%, and 13.3%, respectively. Claudin-7 and claudin-9 overexpression increased claudin-1 and zonula occludens-1 levels. In summary, individual increased expression of claudin-6, claudin-7, or claudin-9 is sufficient to enhance tumorigenic properties of a gastric adenocarcinoma cell line.