Evaluating Disaster Damages and Operational Status of Health-Care Facilities During the Emergency Response Phase of Hurricane Maria in Puerto Rico.

On September 20, 2017, Hurricane Maria made landfall on Puerto Rico as a category 4 storm, resulting in serious widespread impact across the island, including communication and power outages, water systems impairment, and damage to life-saving infrastructure. In collaboration with the Puerto Rico Department of Health, the Public Health Branch (PHB), operating under the Department of Health and Human Services Incident Response Coordination Team, was tasked with completing assessments of health-care facilities in Puerto Rico to determine infrastructure capabilities and post-hurricane capacity. Additionally, in response to significant data entry and presentation needs, the PHB leadership worked with the Puerto Rico Planning Board to develop and test a new app-based infrastructure capacity assessment tool. Assessments of hospitals were initiated September 28, 2017, and completed November 10, 2017 (n = 64 hospitals, 97%). Assessments of health-care centers were initiated on October 7, 2017, with 186 health-care centers (87%) assessed through November 18, 2017. All hospitals had working communications; however, 9% (n = 17) of health-care centers reported no communication capabilities. For the health-care centers, 114 (61%) reported they were operational but had sustainment needs. In conclusion, health-care facility assessments indicated structural damage issues and operational capacity decreases, while health-care centers reported loss of communication capabilities post-Hurricane Maria.

Stereochemical aspects of 1,3-butadiene metabolism and toxicity in rat and mouse liver microsomes and freshly isolated rat hepatocytes.

1,3-Butadiene (BD) is a gas used heavily in the rubber and plastics industry. BD and its epoxide metabolites have been shown to be carcinogenic and mutagenic in rodents, and BD has been classified by IARC as a group 2A carcinogen. We have examined the role of stereochemistry in species-dependent metabolism and toxicity of BD. Diastereo- and enantioselective synthetic routes to butadiene monoxide (BMO), butadiene bisoxide (BBO), and 3,4-epoxybutane-1,2-diol isomers have been developed. These routes have allowed the development of chiral gas chromatographic and GC/MS analytical procedures for quantitation of these metabolites in biological experiments. We have utilized hepatic microsomes from male B6C3F1 mice and hepatic microsomes and intact hepatocytes from male Sprague-Dawley rats as experimental systems. At 30 min, BMO production from BD was two times higher in mouse hepatic microsomes than in rats, and stereoselective analysis was used to determine the relative formation of (R)- and (S)-BMO. Formation of BBO from both (R)- and (S)-BMO was characterized in rat and mouse microsomal systems. As expected, more BBO was formed in mouse hepatic microsomes (3-4-fold) than in rat hepatic microsomes. No difference in total BBO formed from either isomer was observed in rat microsomes, but in mouse microsomes significantly more BBO was produced from (S)-BMO than from (R)-BMO. The cytotoxicity of each BMO and BBO enantiomer was examined in freshly isolated rat hepatocytes. (R)-BMO showed greater cytotoxicity than (S)-BMO. Stereospecific cytotoxicity was also observed using BBO enantiomers and (meso)-BBO was more cytotoxic than either the (R:R) or the (S:S)-BBO. The results show that stereochemistry plays an important role in BD metabolism and cytotoxicity and for the purposes of risk assessment needs to be compared across species.

Metabolism of 1,3-butadiene to butadiene monoxide in mouse and human bone marrow cells.

1,3-Butadiene (BD), a gas used in the production of rubber and plastics, induces a high incidence of leukemias and lymphomas in B6C3F1 mice. Because of the potential involvement of the hematopoietic system in response to BD, we have examined metabolism of BD by B6C3F1 mouse and human bone marrow and by purified human myeloperoxidase (MPO), an enzyme rich in bone marrow. BD was metabolized to butadiene monoxide (BMO) by MPO and by mouse and human bone marrow cells. In all of these systems metabolism was stimulated by hydrogen peroxide suggesting a peroxidase-mediated process. In B6C3F1 mouse bone marrow cell lysates, hydrogen peroxide but not NADPH stimulated metabolism suggesting that cytochrome P450 was not involved in BMO formation. Metabolism of BD to BMO in hydrogen peroxide-fortified mouse bone marrow cell lysates was more than two orders of magnitude lower than in either NADPH-fortified rat or mouse hepatic microsomes. Experiments using both mouse and human bone marrow cells showed that cells from both sources could generate BMO from BD. These data show that BD can be converted to BMO in a target organ of BD carcinogenicity.

Solvolytic formation of 1,2-dichloro-3,4-epoxybutane from butadiene monoxide under physiological conditions.

Butadiene monoxide, a presumed carcinogenic metabolite of butadiene, is stable in water or phosphate buffer, but was found to rapidly disappear from the headspace of solutions (10(-6) to 10(-4) M) in phosphate-buffered saline incubated at 37 degrees C. The process was first order with respect to monoxide concentration, with an apparent rate constant of 6.6 x 10(-4) sec-1. Mass spectrometric examination of the major product formed indicated it to be 1,2-dichloro-3,4-epoxybutane, which was confirmed by synthesis. Formation of the dichloro epoxide was linearly dependent on chloride ion concentration of the medium, but independent of dissolved oxygen. The formation of the dichloro epoxide is explained by slow solvolytic formation of a chloronium ion from butadiene monoxide, which is followed by attack of chloride ion to generate chlorine and butadiene. The chlorine is than rapidly trapped by second molecule of butadiene monoxide. This was confirmed by competitive trapping of generated chlorine by inclusion of crotyl alcohol in the incubation. A similar pathway has recently been demonstrated for reversible formation of bromine from solvolytically generated bromonium ions. The facile formation of dichloroepoxybutane under physiological conditions may be of significance in the toxicity of butadiene.