Inorganic mercury, in the form of mercurous chloride, or calomel, is intentionally added to some cosmetic products sold through informal channels in Mexico and the US for skin lightening and acne treatment. These products have led to multiple cases of mercury poisoning but few investigations have addressed the contamination of cream users’ homes. We report on several cases of mercury poisoning among three Mexican-American families in California from use of mercury-containing skin creams. Each case resulted in widespread household contamination and secondary contamination of family members. Urine mercury levels in cream users ranged from 37 to 482 µg/g creatinine and in non-users from non-detectable to 107 µg/g creatinine. Air concentrations of up to 8 µg/m3 of mercury within homes exceeded the USEPA/ATSDR health-based guidance and action level of <1.0 μg/m3. Mercury contamination of cream users’ homes presented a multi-pathway exposure environment to residents. Homes required extensive decontamination, including disposal of most household items, to achieve acceptable air levels. The acceptable air levels used were not designed to consider multi-pathway exposure scenarios. These findings support that the calomel is able to change valence form to elemental mercury and volatilize once exposed to the skin or surfaces in the indoor environment.

Our hypothesis that multidimensional EOL care preferences would differ based on hypothetical death scenarios was partially supported and suggests the need for disease-specific EOL care discussions.

Because personal values do influence EOL preferences, care should be taken to ascertain patient values when presenting diagnoses, prognoses, and treatment options. In particular, patients and families of patients with progressive neurological diseases will likely face a time when the patient cannot self-represent EOL wishes. Early discussion of values and preferences, particularly in the context of cognitive disease is vital to assure patient-directed care.

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We were able to demonstrate type I1 collagen in synovial phagocytes of osteoarthritis (OA) and rheumatoid arthritis (RA) patients, using a monoclonal antibody to human type I1 collagen and immunoperoxidase staining. In addition, using immunoelectron microscopy, we demonstrated labeled fragments in synovial phagocytes of both RA and OA patients. This immunohistoehemical assay may prove to be a sensitive indicator of cartilage erosion in patients with OA and RA.There is currently no sensitive indicator of active cartilage destruction in patients with arthritis. Radiographs provide only a historical record of severe damage. Clinical assessment of osteoarthritis (OA) and rheumatoid arthritis (RA) is also often inadequate; subjective assessment of pain is often the measurement used. Laboratory tests, such as erythrocyte sedimentation rate (ESR) and C-reactive protein values, are indirect measures of joint inflammation. In an effort to find markers for cartilage and joint destruction in various forms of connective tissue diseases, numerous investigators have studied bone and cartilage components, such as hydroxyproline (l), pyridinoline (2), type 111 procollagen peptide (3), proteoglycans (4), and cartilage matrix glycoprotein (3, in serum and urine. However, none of these investigations has thus far led to wider clinical use and application.Of the 5 main components of cartilage, i.e., collagen, proteoglycans, water, noncollagenous proteins, and cells, type I1 collagen makes up about half the dry weight of adult articular cartilage (6). Based on the fact that normal synovial fluid (SF) does not contain collagen, the existence of type I1 collagen in SF indicates either current ongoing or recent degradation of articular cartilage. With this in mind, we sought to detect type I1 collagen in synovial phagocytes and SF of patients with RA and OA using a monoclonal antibody (MAb) directed against human type I1 collagen. The ability to identify type I1 collagen in SF may be helpful not only in evaluating the extent of initial joint damage, but also in following the progression of joint disease.