Abstract:There have been several epidemiological and experimental studies about styrene from the neuroendocrinological viewpoint. Some reported that styrene exposure affected the neuroendocrinological system and enhanced prolactin (PRL) secretion, but others have denied those effects. It was assumed that styrene exposure caused depletion of dopamine (DA), which is a PRL inhibitor, and that, in consequence, the PRL level increased. However, not only DA but also many other factors control PRL secretion. Therefore, the me… Show more
“…The only known physiological function of prolactin is the stimulation of milk production and many normal stress situations may lead to elevations without any chemical exposure (Theorell et al 1990). Although screening or guideline studies do not exist for experimental verification of the human observations, mechanistic studies in animal on dopamine, the prolactin-regulating neurotransmitter, do not support an explanation of how styrene may affect prolactin levels (Gagnaire et al 2006;Jarry et al 2002;Umemura et al 2005). Therefore, given the lack of a plausible mechanistic explanation, coupled with the nature of the changes, unspecific acute workplace-related stress is a possible alternative explanation to styrene exposure in these workers.…”
The potential chronic health risks of occupational and environmental exposure to styrene were evaluated to update health hazard and exposure information developed since the Harvard Center for Risk Analysis risk assessment for styrene was performed in 2002. The updated hazard assessment of styrene's health effects indicates human cancers and ototoxicity remain potential concerns. However, mechanistic research on mouse lung tumors demonstrates these tumors are mouse-specific and of low relevance to human cancer risk. The updated toxicity database supports toxicity reference levels of 20 ppm (equates to 400 mg urinary metabolites mandelic acid + phenylglyoxylic acid/g creatinine) for worker inhalation exposure and 3.7 ppm and 2.5 mg/kg bw/day, respectively, for general population inhalation and oral exposure. No cancer risk value estimates are proposed given the established lack of relevance of mouse lung tumors and inconsistent epidemiology evidence. The updated exposure assessment supports inhalation and ingestion routes as important. The updated risk assessment found estimated risks within acceptable ranges for all age groups of the general population and workers with occupational exposures in non-fiber-reinforced polymer composites industries and fiber-reinforced polymer composites (FRP) workers using closedmold operations or open-mold operations with respiratory protection. Only FRP workers using open-mold operations not using respiratory protection have risk exceedances for styrene and should be considered for risk management measures. In addition, given the reported interaction of styrene exposure with noise, noise reduction to sustain levels below 85 dB(A) needs be in place.
“…The only known physiological function of prolactin is the stimulation of milk production and many normal stress situations may lead to elevations without any chemical exposure (Theorell et al 1990). Although screening or guideline studies do not exist for experimental verification of the human observations, mechanistic studies in animal on dopamine, the prolactin-regulating neurotransmitter, do not support an explanation of how styrene may affect prolactin levels (Gagnaire et al 2006;Jarry et al 2002;Umemura et al 2005). Therefore, given the lack of a plausible mechanistic explanation, coupled with the nature of the changes, unspecific acute workplace-related stress is a possible alternative explanation to styrene exposure in these workers.…”
The potential chronic health risks of occupational and environmental exposure to styrene were evaluated to update health hazard and exposure information developed since the Harvard Center for Risk Analysis risk assessment for styrene was performed in 2002. The updated hazard assessment of styrene's health effects indicates human cancers and ototoxicity remain potential concerns. However, mechanistic research on mouse lung tumors demonstrates these tumors are mouse-specific and of low relevance to human cancer risk. The updated toxicity database supports toxicity reference levels of 20 ppm (equates to 400 mg urinary metabolites mandelic acid + phenylglyoxylic acid/g creatinine) for worker inhalation exposure and 3.7 ppm and 2.5 mg/kg bw/day, respectively, for general population inhalation and oral exposure. No cancer risk value estimates are proposed given the established lack of relevance of mouse lung tumors and inconsistent epidemiology evidence. The updated exposure assessment supports inhalation and ingestion routes as important. The updated risk assessment found estimated risks within acceptable ranges for all age groups of the general population and workers with occupational exposures in non-fiber-reinforced polymer composites industries and fiber-reinforced polymer composites (FRP) workers using closedmold operations or open-mold operations with respiratory protection. Only FRP workers using open-mold operations not using respiratory protection have risk exceedances for styrene and should be considered for risk management measures. In addition, given the reported interaction of styrene exposure with noise, noise reduction to sustain levels below 85 dB(A) needs be in place.
“…In fact, prolactin can be increased by exposure to lead (Govoni et al 1987;Lucchini et al 2000), organic mercury (Carta et al 2003), and manganese (Ellingsen et al 2003;Smargiassi and Mutti 1999;Takser et al 2004), but it can be decreased by exposure to inorganic mercury Lucchini et al 2003;Ramalingam et al 2003), alluminum (Alessio et al 1989), and cadmium (Calderoni et al 2005;). Subjects exposed to chemicals such as styrene (Bergamaschi et al 1996;Luderer et al 2004;Umemura et al 2005), perchloroethylene (Beliles 2002;Ferroni 1992), and anesthetic gases (Lucchini et al 1996;(Marana et al 2003) have shown an increase of serum prolactin, whereas polychlorinated biphenyls (De Krey et al 1994) Possible mechanisms, other than direct effects at the cellular level, may be related to different neurotransmitters involved in the modulation of prolactin secretion. For example, the dopaminergic and serotoninergic systems, respectively, are involved in the physiologic regulation of this hormone as a tonic inhibitor and as an excitatory modulator.…”
Section: Prolactin Changes As a Consequence Of Chemical Exposurementioning
“…Increases in serum growth hormone and TSH were also observed and were associated with biomarkers of styrene exposure (13)(14)(15)(16). Toxicological studies on rats also support prolactin secretion as a styrene target, with sex-related differences (17). An up-to-date, comprehensive review of health effects and exposure to styrene is available (18).…”
Chronic exposure to styrene is not associated with an increase in nodular or autoimmune thyroid diseases. However, styrene could interfere with peripheral metabolism of thyroid hormones by inhibiting T(4) to T(3) conversion. Whether this is a direct effect on iodothyronine deiodinases or a consequence of a general distress, such as in nonthyroidal illnesses, remains to be established. Further studies in a larger population of exposed workers are needed to confirm these preliminary observations.
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