Increased living temperature alters the cardiopulmonary response of male and female mice to benzene-toluene-ethylbenzene-xylene (BTEX)
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Benzene, toluene, ethylbenzene, and xylene (BTEX) compounds are ubiquitous in the environment, originating from both natural and anthropogenic sources. Despite the broad presence of BTEX in the environment, extensive use of petroleum products and improper maintenance of underground storage tanks (USTs) have increased the risk of exposure to these compounds. Hazardous substances stored in USTs, like BTEX, may leak into groundwater, soil, and buildings and homes over time. Furthermore, higher temperatures exacerbate the release of VOCs. Therefore, the purpose of this study was to characterize the cardiopulmonary effects of inhaled BTEX in female and male C57BL6J mice and assess the role of living temperature.
Eight-week-old mice were housed at normal temperature (NT - 22°C) or high temperature (HT - 32°C) for five weeks. Mice were then exposed to either filtered air (FA) or BTEX (nose-only) for four hours per day for two consecutive days. Ventilatory function was assessed via whole-body plethysmography (WBP) one day before and immediately after the first exposure. High-frequency echocardiography (HF-echo) was performed the week prior to exposure and again immediately following the second exposure. WBP and HF-echo measurements were compared from pre- to post-exposure.
When compared to NT, HT significantly increased tidal volume (TV), peak expiratory flow (PEF) peak inspiratory flow (PIF), and relaxation time (RT), and decreased enhanced pause (Penh) in female and male mice. BTEX increased frequency (f) and decreased expiratory and inspiratory times (Te and Ti, respectively) as well as Penh in female NT mice but had no effect on male NT mice. At HT, BTEX significantly decreased f and Penh and increased TV, Te, Ti, and RT in female mice, and only increased TV, PEF, PIF in males. Thus, the impact of HT and BTEX on female mice appeared to be greater than on males.
Female HT-FA mice had a significant decrease in heart rate (HR) compared to NT, while BTEX caused an increase. On the other hand, male FA mice experienced an increase in HR at HT. No significant differences in cardiac output, stroke volume, fractional shortening, ejection fraction, end systolic volume, or end diastolic volume were observed between the groups. These results indicate that higher living temperature alters cardiopulmonary function in female and male mice in a differential manner. Although breathing changes seem to be largely driven by temperature, it is worth noting that HT might contribute to a higher inhaled BTEX dose, and therefore, increased risk. Long-term exposure assessments are needed to clarify these effects further.