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Low-level lead exposure increases blood pressure and may increase the risk of hypertension.

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Reactive oxygen species (ROS) are implicated in the regulation of apoptosis through a number of distinct mechanisms depending on cell type and stimulation conditions. Glyoxalase I (GI) metabolizes methylglyoxal (MG) and MG-derived advanced glycation end products (AGEs) known to cause apoptosis. This study examined the possible role of GI among the mechanisms of ROS-driven apoptosis in human bronchial epithelial BEAS-2B cells exposed to wood dust and signaling pathways by which these reactive species regulate GI expression. Our results showed that wood dust generated distinct ROS (superoxide anion, and hydrogen peroxide) by selectively inhibiting the enzymatic activity of superoxide dismutase or glutathione peroxidase and catalase enzymes. These ROS caused a dramatic inhibition of the antiglycation GI enzyme, leading to the intracellular accumulation of the pro-apoptotic AGE, argpyrimidine (AP) and programmed cell death via a mitochondrial pathway. Pre-treatment with N-acetyl-L-cysteine (NAC), a ROS scavenger, prevented these events. Hence, ROS-induced apoptosis in BEAS-2B cells occurred via a novel mechanism relying on GI inhibition and AP accumulation. We interestingly found that superoxide anion and hydrogen peroxide induced a diverse apoptosis level by differently inhibiting GI via NF-κB pathway. Since maintenance of an intact epithelium is a critically important determinant of normal respiratory function, the knowledge of the mechanisms underlying its disruption may provide insight into the genesis of a number of pathological conditions commonly occurring in wood dust occupational exposure. Our findings suggest that the antioxidant NAC may merit investigation as a potential preventive agent in wood dust exposure-induced respiratory diseases.

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Chronic obstructive pulmonary disease (COPD) is caused by exposure to noxious particles and gases. Smoking is the main risk factor, but other factors are also associated with COPD. Occupational exposure to vapours, gases, dusts and fumes contributes to the development and progression of COPD, accounting for a population attributable fraction of 14%. Workplace pollutants, in particular inorganic dust, can initiate airway damage and inflammation, which are the hallmarks of COPD pathogenesis. Occupational COPD is still underdiagnosed, mainly due to the challenges of assessing the occupational component of the disease in clinical settings, especially if other risk factors are present. There is a need for specific education and training for clinicians, and research with a focus on evaluating the role of occupational exposure in causing COPD. Early diagnosis and identification of occupational causes is very important to prevent further decline in lung function and to reduce the health and socio‐economic burden of COPD. Establishing details of the occupational history by general practitioners or respiratory physicians could help to define the occupational burden of COPD for individual patients, providing the first useful interventions (smoking cessation, best therapeutic management, etc.). Once patients are diagnosed with occupational COPD, there is a wide international variation in access to specialist occupational medicine and public health services, along with limitations in workplace and income support. Therefore, a strong collaboration between primary care physicians, respiratory physicians and occupational medicine specialists is desirable to help manage COPD patients' health and social issues.

From 22 March until 18 May 2020, a complete lockdown in Italy was ordered as a countermeasure against the COVID-19 pandemic. Social isolation measures affect some populations more than others, and people with drug and/or alcohol disorders (SUDs) are more likely to be adversely affected. This study presents, for the first time, laboratory data on the use of alcohol and drugs in a high-risk population during Italy’s first wave of the COVID-19 pandemic. Thirty subjects with SUDs were monitored for the use of illicit drugs and alcohol every 3 months before, during and after the lockdown, by hair analysis. The number of samples positive for heroin, cocaine, MDMA and cannabis fell considerably during the lockdown and then resumed to pre-lockdown levels when the period of confinement was over. Interestingly, the consumption of benzodiazepines and alcohol followed the opposite trend; both the number of benzodiazepine-positive samples and the level of alcohol consumption increased and remained high, even at the end of the lockdown. The confinement measures produced significant changes in drug/alcohol use patterns, with a shift toward the use of substances that were more easily accessible, used as self-medication for negative feelings, and used to alleviate the effects of abstinence from drugs that were no longer readily available.