Gender Disparities in Occupational Health
Over the past few decades, the presence of women in the workforce has changed significantly. According to the US Bureau of Labor Statistics Current Population Survey, in 2015, 46.8% of the workforce included women compared with 28.6% in 1948. Along with this change, there has been an increased focus on gender disparities in occupational health.
Gender differences in occupational asthma were also seen in snow crab processing plant workers. Women were significantly more likely to have occupational asthma than men. However, they found that overall, women had a greater cumulative exposure to crab allergens, which may be a major contributor to this disparity (Howse et al. Environ Res. 2006;101:163).
Although several occupational health studies are beginning to highlight gender disparities, a major confounding factor is that of occupational segregation, meaning the under-representation of one gender in some jobs and over-representation in others. Differences in jobs and tasks even within the same job title between men and women are often major contributors to gender disparities [WHO Dept of Gender, Women and Health, 2006]. Also, several studies suggest that more women should be included in toxicology and occupational cancer studies, since currently, they have included mostly men (Sorrentino et al. Ann Ist Super Sanità. 2016;52:190). Perhaps future studies can improve the overall understanding of these important contributing factors to gender disparities in occupational health.
Krystal Cleven, MD
Does Beta-agonist Therapy With Albuterol Cause Lactic Acidosis?
Cohen and associates (Clin Sci Mol Med. 1977;53:405) suggested that lactic acidosis can occur in at least two different physiologic clinical presentations. Type A occurs when oxygen delivery to the tissues is compromised. Dodda and Spiro (Respir Care. 2012;57:2115) indicated that type A lactic acidosis was due to hypoxemia, as seen in inadequate tissue oxygenation during an exacerbation of asthma. In severe asthma, pulsus paradoxus and air trapping (causing intrinsic positive end-expiratory pressure, or PEEP) served to decrease tissue oxygenation by decreasing cardiac output and venous return, leading to type A lactic acidosis. Bates and associates (Pediatrics. 2014;133:e1087) considered the role of intrapulmonary arteriovenous anastomoses (IPAVs) when a status asthmaticus patient improved after cessation of beta-agonist therapy. Type B lactic acidosis occurs when lactate production was increased or lactate removal was decreased even when oxygen was delivered to tissue. Amaducci (http://www.emresident.org/gasping-air-albuterol-induced-lactic-acidosis/) explained how high dosages of albuterol, beyond 1 mg/kg, created an increased adrenergic state that, with reduced tissue perfusion, increased glycolysis and pyruvate production, resulting in measurable hyperlactatemia. The authors (Br J Med Pract. 2011;4:a420) noted that lactic acidosis also occurs in acute severe asthma due to inadequate oxygen delivery to the respiratory muscles to meet an elevated oxygen demand or due to fatiguing respiratory muscles. Ganaie and Hughes reported a case of lactic acidosis caused by treatment with salbutamol. Salbutamol is the most commonly used short-acting beta-agonist. Stimulation of beta-adrenergic receptors leads to a variety of metabolic effects, including increase in glycogenolysis, gluconeogenesis, and lipolysis, thus contributing to lactic acidosis. All authors agreed that the mechanism of albuterol-caused lactic acidosis was poorly understood.
Douglas E. Masini, EdD, FCCP
Steering Committee Member
Withdrawal of OSA Screening Regulation for Commercial Motor Vehicle Operators
Compared with the general US population, the prevalence of sleep apnea (SA) is higher among commercial motor vehicle (CMV) drivers (Berger et al. J Occup Environ Med. 2012;54:1017). Additionally, the risk of motor vehicle accidents is higher among individuals with SA compared with those without SA (Tregear et al. J Clin Sleep Med. 2009;5:573), and treatment of SA is associated with a reduction in this risk (Mahssa et al. Sleep. 2015;38341).
However, after reviewing the public input and data, the FRA and FMCSA recently announced that there was “not enough information available to support moving forward with a rulemaking action,” and, therefore, they are no longer pursuing the regulation that would require SA screening for truck drivers and train engineers (Federal Register August 2017;49 CFR 391,240,242). See CHEST’s press release at www.chestnet.org/News/Press-Releases/2017/08/American-College-of-Chest-P.... The FMCSA endorses existing resources,such as the North American Fatigue Management Program (NAFMP) (www.nafmp.org), which is a web-based program designed to reduce driver fatigue and includes information on SA screening and treatment. The medical examiners, however, will have the ultimate responsibility to screen, diagnose, and treat SA based on their medical knowledge and clinical experience.
Vaishnavi Kundel, MD
Steering Committee Member
Corrections to previous NetWork articles
Mohsin Ijaz’s name was misspelled.
The name under Shruti Gadre’s photograph is wrong. It says Dr. Ahya instead of Dr. Gadre.
The authorship of the article at the end of the article is incorrect. It says Vivek Ahya, instead of Shruti Gadre and Marie Budev.