Urban penalty y reforma sanitaria: el caso de una ciudad minera: La Unión (1870-1913) / Urban penalty and health reform. The case of a mining city: La Unión (1870-1913)

Este trabajo consta de tres partes. En la primera, proponemos analizar la urban penalty desde la óptica de los fallos de mercado. En la segunda parte, ofrecemos datos que evidencian que La Unión sufrió urban penalty entre 1870 y la Primera Guerra Mundial. En la tercera parte, cuantificamos el gasto que se invirtió en la reforma sanitaria de la ciudad y documentamos que no se instalaron cámaras de condensación en las fundiciones de plomo que existían en el casco urbano pese a que la legislación así lo exigía. Para terminar, sostenemos que La Unión sufrió urban penalty hasta la Primera Guerra Mundial porque el gasto en reforma sanitaria fue insuficiente y no se instalaron esas cámaras de condensación. Uno y otro hecho se explican por razones políticas. La ciudad estuvo gobernada por una oligarquía de empresarios dueños de minas y fundiciones poco sensibles a los problemas sociales que invirtió en salud pública menos que otras ciudades españolas de población similar y que utilizó recursos públicos para fines privados. Esa misma oligarquía no cumplió con la legislación que obligaba a introducir en las fábricas de plomo cámaras de condensación

In the first part of this article, we analyze urban penalty from the perspective of market failures. In the second part, we offer data showing that La Union suffered urban penalty between 1870 and the First World War. Finally, in the third part, we quantify the expenditure invested by the city in health reform and document the failure to install condensation chambers in lead smelters in the city, despite this being a legal requirement. In conclusion, we support the hypothesis that the Union suffered an urban penalty up to the First World War because spending on health reform was insufficient and condensation chambers were not installed, which both have political explanations. The city was ruled by an oligarchy of business men, owners of mines and smelters and insensitive to the social problems. Less was invested in public health in comparison to other Spanish cities with similar populations, and public resources were used for private purposes. This same oligarchy did not comply with the state legislation requiring the introduction of condensation chambers in lead factories

Lead poisoning and other human-related factors cause significant mortality in white-tailed eagles.

The white-tailed eagle (Haliaeetus albicilla) suffered a severe population decline due to environmental pollutants in the Baltic Sea area ca. 50 years ago but has since been recovering. The main threats for the white-tailed eagle in Finland are now often related to human activities. We examined the human impact on the white-tailed eagle by determining mortality factors of 123 carcasses collected during 2000-2014. Routine necropsy with chemical analyses for lead and mercury were done on all carcasses. We found human-related factors accounting for 60% of the causes of death. The most important of these was lead poisoning (31% of all cases) followed by human-related accidents (e.g. electric power lines and traffic) (24%). The temporal and regional patterns of occurrence of lead poisonings suggested spent lead ammunition as the source. Lead shot was found in the gizzards of some lead-poisoned birds. Scavenging behaviour exposes the white-tailed eagle to lead from spent ammunition.

Mortality of lead smelter workers: A follow-up study with exposure assessment.

BACKGROUND: Lead exposure has been linked to impaired renal function and kidney failure. High lead exposures have been associated with increased mortality from certain cancers, hypertension, cardiovascular disease, and amyotrophic lateral sclerosis (ALS). METHODS: We extended vital status follow-up on a cohort of 1,990 lead smelter workers by 25 years and computed standardized mortality ratios and rate ratios (RR) stratified by cumulative lead exposure. RESULTS: The update added 13,823 person-years at risk and 721 deaths. Increased risk of mortality was observed for the a priori outcomes of lung cancer, cardiovascular disease (including cerebrovascular disease), chronic kidney disease, and ALS. However, of these outcomes, only cardiovascular, cerebrovascular, and chronic kidney diseases were associated with a positive exposure-response in RR analyses. CONCLUSIONS: This study reaffirms the association of lead exposure with cardiovascular and kidney diseases; however, increased mortality observed for certain cancers is not likely to be due to lead exposure. Am. J. Ind. Med. 59:979-986, 2016. Published 2016. This article is a U.S. Government work and is in the public domain in the USA.

Blood Lead Levels and Cause-Specific Mortality of Inorganic Lead-Exposed Workers in South Korea.

The objective of this study was to identify the association of blood lead level (BLL) with mortality in inorganic lead-exposed workers of South Korea. A cohort was compiled comprising 81,067 inorganic lead exposed workers working between January 1, 2000, and December 31, 2004. This cohort was merged with the Korean National Statistical Office to follow-up for mortality between 2000 and 2008. After adjusting for age and other carcinogenic metal exposure, all-cause mortality (Relative risk [RR] 1.36, 95% confidence interval [CI] 1.03-1.79), digestive disease (RR 3.23, 95% CI 1.33-7.86), and intentional self-harm (RR 2.92, 95% CI 1.07-7.81) were statistically significantly higher in males with BLL >20 µg/dl than of those with BLL ≤10µg/dl. The RR of males with BLL of 10-20 µg/dl was statistically higher than of those with BLL ≤10µg/dl in infection (RR 3.73. 95% CI, 1.06-13.06). The RRs of females with 10-20 µg/dl BLL was statistically significantly greater than those with BLL <10µg/dl in all-cause mortality (RR 1.93, 95% CI 1.16-3.20) and colon and rectal cancer (RR 13.42, 95% CI 1.21-149.4). The RRs of females with BLL 10-20 µg/dl (RR 10.45, 95% CI 1.74-62.93) and BLL ≥20 µg/dl (RR 12.68, 95% CI 1.69-147.86) was statistically significantly increased in bronchus and lung cancer. The increased suicide of males with ≥20 µg/dl BLLs, which might be caused by major depression, might be associated with higher lead exposure. Also, increased bronchus and lung cancer mortality in female workers with higher BLL might be related to lead exposure considering low smoking rate in females. The kinds of BLL-associated mortality differed by gender.

[The Cause of Death of the Emperor Meiji's Infants].

The Emperor Meiji had fifteen children, including five princes and ten princesses, but ten of them died of meningitis-like disease in their infancy. Those involved in the situation were apprehensive about reporting on circumstances that might suggest that the lineage of the imperial family was in a critical condition. The author considers that this disease was caused by the facial powder containing white lead used by wet-nurses.

High concentration of blood lead levels among young children in Bagega community, Zamfara - Nigeria and the potential risk factor.

INTRODUCTION: In May 2010, lead poisoning (LP) was confirmed among children <5years (U5) in two communities in Zamfara state, northwest Nigeria. Following reports of increased childhood deaths in Bagega, another community in Zamfara, we conducted a survey to investigate the outbreak and recommend appropriate control measures. METHODS: We conducted a cross-sectional survey in Bagega community from 23rd August to 6th September, 2010. We administered structured questionnaires to parents of U5 to collect information on household participation in ore processing activities. We collected and analysed venous blood samples from 185 U5 with LeadCare II machine. Soil samples were analysed with X-ray fluorescence spectrometer for lead contamination. We defined blood lead levels (BLL) of >10ug/dL as elevated BLL, and BLL ≥45ug/dL as the criterion for chelation therapy. We defined soil lead levels (SLL) of ≥400 parts per million (ppm) as elevated SLL. RESULTS: The median age of U5 was 36 months (Inter-quartile range: 17-48 months). The median BLL was 71µg/dL (range: 8-332µg/dL). Of the 185 U5, 184 (99.5%) had elevated BLL, 169 (91.4%) met criterion for CT. The median SLL in tested households (n = 37) of U5 was 1,237ppm (range: 53-45,270ppm). Households breaking ore rocks within the compound were associated with convulsion related-children's death (OR: 5.80, 95% CI: 1.08 - 27.85). CONCLUSION: There was an LP outbreak in U5 in Bagega community possibly due to heavy contamination of the environment as a result of increased ore processing activities. Community-driven remediation activities are ongoing. We recommended support for sustained environmental remediation, health education, intensified surveillance, and case management.

Anemias sideroblásticas y puenteado basófilo: Indicador biológico por exposición ocupacional al plomo y sus derivados / Sideroblastic anemia and basophilic bridged: Biological indicator of occupational exposure to lead and its derivatives

En el presente estudio se evaluaron 34 individuos de ambos géneros (n = 15 mujeres y n = 19 hombres) con edades promedios de 37,35 ± 10,37. De los cuales 09 trabajadores de talleres mecánicos y 25 de imprentas gráficas con exposición laboral entre 8 a 10 horas/día. Bajo su consentimiento se les tomo muestra de sangre del antebrazo derecho para evaluar hematológica y morfológicamente glóbulos rojos (punteado basófilo), glóbulos blancos (segmentados neutrofilos), plaquetas y determinar por espectroscopia de absorción atómica con atomización elec trotérmica niveles séricos de plomo. Los resultados analíticos obtenidos para niveles de plomo globales expresados en μgL-1 de 36,03 ± 23,02 evidenciaron correlación directa y positiva con los parámetros bioquímicos evaluados. Ma yo res concentraciones de plomo en sangre coincidieron con pun teados basófilos toscos y alteraciones cualitativas morfológicas tales como hipocromía moderada en glóbulos rojos, granulaciones tóxicas e hipersegmentación en segmentados neutrofilos. No se observaron diferencias estadísticamente significativas con un p = 0,002 entre los grupos expuestos y tiempo de exposición por jornada laboral, más si entre los géneros con un p = 0,087, siendo más evidente el impacto de la exposición ocupacional en hombres, asumiendo mayor masa corporal y por ende mayor densidad ósea por donde este metal tóxico tiene un 95% de afinidad, además de contar el género masculino con mayor producción hematopoyética (La cantidad considerada normal fluctúa entre 4.500.000 (en la mujer) y 5.000.000 (en el hombre) por milímetro cúbico (o microlitro) de sangre). Los resultados obtenidos constituyen una herramienta útil para un pre-diagnóstico a exposición o intoxicación por plomo cuando por infraestructura no se cuente en laboratorios bioanalíticos con un equipo de espectroscopia de ab sorción atómica con atomización electrotérmica.

This study assessed 34 individuals of both genre (n = 15 women and n = 19 men) aged averages of 37.35 ± 10.37. Of whom 09 workers of garages and 25 printing graphs with occupational exposure between 8 to 10 hours per day. Under their consent took them right forearm blood sample to evaluate haematological and morphologically (stippling Basophilic) red blood cells, white blood cells (segmented neutrophils), pla te lets and by Atomic Spectrometry atomization absorption spectroscopy to determine serum levels of lead. The analytical re sults for overall lead levels ex pressed in μgL-1 36.03 ± 23.02 demonstrate positive and direct correlation with the biochemical parameters evaluated. High concentrations of lead in blood coincided with various crude basophiles and qualitative morphological alterations such as hypochromia moderate red globules, toxic granulation’s and hypersegmentation in segmented neutrophils. There were no statistically significant differences with p = 0.002 among exposed groups and exposure time by working day, more if genre with a p = 0.087, being most evi dent impact of occupational exposure in men, assuming greater mass body and therefore greater bone density where this toxic metal has a 95% of affinity’s well as the masculine gender with greater production hematopoietic (considered normal amount fluctuates between 4.500.000 (in women) and 5.000.000 (in humans) per cubic millimeter (microliter) of blood). The results constitute a useful tool for an prediag nostic to exposure or poisoning by lead when infrastructure don’t count in laboratories bioanalytic’s with a team of atomic absorption spectroscopy with spectrometry atomization.

Patterns of mortality in free-ranging California Condors (Gymnogyps californianus).

We document causes of death in free-ranging California Condors (Gymnogyps californianus) from the inception of the reintroduction program in 1992 through December 2009 to identify current and historic mortality factors that might interfere with establishment of self-sustaining populations in the wild. A total of 135 deaths occurred from October 1992 (the first post-release death) through December 2009, from a maximum population-at-risk of 352 birds, for a cumulative crude mortality rate of 38%. A definitive cause of death was determined for 76 of the 98 submitted cases, 70% (53/76) of which were attributed to anthropogenic causes. Trash ingestion was the most important mortality factor in nestlings (proportional mortality rate [PMR] 73%; 8/11), while lead toxicosis was the most important factor in juveniles (PMR 26%; 13/50) and adults (PMR 67%; 10/15). These results demonstrate that the leading causes of death at all California Condor release sites are anthropogenic. The mortality factors thought to be important in the decline of the historic California Condor population, particularly lead poisoning, remain the most important documented mortality factors today. Without effective mitigation, these factors can be expected to have the same effects on the sustainability of the wild populations as they have in the past.

Acute lead toxicosis via ingestion of spent ammunition in a free-ranging cougar (Puma concolor).

Lead toxicity has long been documented and acknowledged as a significant health issue of water birds and avian scavengers. However, few instances of toxic effects to higher mammalian carnivores have been documented. Here we present an acute case of lead toxicity in a free-ranging cougar (Puma concolor) in Oregon.

Risk of single and combined exposure of birds to non-steroidal anti-inflammatory drugs and lead.

OBJECTIVES: Pharmaceuticals and heavy metals such as diclofenac and lead, respectively, have been identified as environmental contaminants toxic to birds and posing serious threats to declining populations of raptors worldwide. The aim of the present study was to test the hypothesis that a sublethal combination of non-steroidal anti-inflammatory drugs and lead induces more pronounced effects than single exposures in birds. METHODS: A total of 40 Japanese quails (Coturnix coturnix japonica) at the age of 2 months and average weight of 180g were on a random basis divided into four experimental groups of 10 specimens (i.e., control, diclofenac, lead, and lead+diclofenac exposures). Six lead shots in the total weight of 1.5 grams were inserted into the crop on day 0 of the experiment, while a total of 5 mg/kg of diclofenac administered intramuscularly were divided into treatments on days 0 and 5. Group responses were compared using haematology and biochemistry after 10 days. RESULTS: There was no mortality in control and both single and combined diclofenac and lead exposure groups, nor did the birds show any clinical signs of intoxication. Univariate analyses of blood parameters yielded a decrease in haematocrit in birds exposed to both substances when compared with the control, a lower haemoglobin level of the lead-exposed group, increased activity of aspartate aminotransferase in the NSAIDs-exposed group, increased activity of alkaline phosphatase in birds exposed to a combination of diclofenac and lead, and a higher phosphorus level in the lead-exposed group. The principal component analysis revealed no multivariate pattern of responses of blood parameters and did not allow separation of exposure groups from controls when the variables and samples were projected onto a two dimensional space. CONCLUSIONS: Results of the present study can enhance understanding of combination toxicity of veterinary drugs and heavy metals in birds, i.e. a scenario that has become environmentally relevant in recent decades. Fortunately, individual blood parameter effects prevailed and no joint mortal effects were recognised in Japanese quails exposed to a combination of sublethal doses of diclofenac and lead.

Vermeer: los colores tóxicos del plomo y del mercurio / Vermeer: the toxic colours of lead and mercury

¿Qué sucede con Vermeer?, se preguntan los historiadores y amantes del arte. El enigmático pintor permaneció en la oscuridad después de su muerte hasta el siglo XIX, en donde capturaría la imaginación y el gusto estético de los tiempos modernos. Aunque han llegado a nosotros sólo treinta y seis de sus obras, su originalidad y refinamiento le colocan entre los más grandes artistas holandeses del siglo XVII. La vida de Vermeer sólo puede recompuesta a través de actas notariales y su dramático final es conocido por boca de su viuda. Nosotros pretendemos aportar un nuevo punto de vista de las razones de su muerte a causa de una intoxicación por plomo y mercurio, y las repercusiones que esta causa tuvo en su pintura (AU)

What is it about Johannes Vermeer? contemporary art lovers and historians ask. The enigmatic painter lapsed into obscurity after his death only to surface again in the 19th century and capture the imagination and esthetic taste of modern times. Even though he produced no more than 40 paintings, their originality and refinement place him among the greatest 17th-century Dutch artists. Vermeer's life story can only be patched together from public records, and the dramatic end of Vermeer`s life was told by his widow after his death.We contribute our point of view of the reason of his death because of a poisoning for lead and mercury and the repercussions that it had in his painting (AU)

Mortality factors and lead contamination of wild birds from Korea.

Wild birds have frequently been found dead in their natural habitats, but little is known about what ecological stressors may impact health of wild populations. Here, we report the potentially harmful lead (Pb) levels in tissues along with necropsies on 69 individuals of cranes, raptors, and waterfowl found dead between 2000 and 2003 in Korea. In all samples diagnosed, trauma (n = 22), severe emaciation (n = 15), and infectious diseases (n = 11) were identified. In the survey, injury with Pb shot or bullet fragments was associated with three of the deaths; one of three showed lesions suggestive of Pb poisoning in the tissues. Of 69 birds, 12 had >25 ppm dry wt. (equivalent to 8 ppm wet wt.) in liver or kidney, which is known to be a potentially lethal level of Pb in wild birds. Three individuals had hepatic Pb levels of 101.3 ppm (Whooper swan), 120.4 ppm (Great white-fronted goose), and 1,059 ppm (Mandarin duck), with evidence of Pb pellets in their gizzard. This study suggests that many birds examined may be suffering from excessive Pb exposure that may be of health concern with respect to a potential cause of their mortality. The need for additional research is heightened when considering that some migrants are classified as a globally protected species by the International Union for the Conservation of Nature.

Evidence of lead exposure in a free-ranging population of Kea (Nestor notabilis).

Kea (Nestor notabilis) are high country parrots endemic to New Zealand. The foraging behavior and inquisitive nature of Kea have led to incidences of foreign substance ingestion, including lead. Between April 2006 and November 2007, 38 Kea in Aoraki/Mount Cook National Park, New Zealand, were captured, and blood was sampled for blood lead analysis. All birds sampled had detectable blood lead with concentrations ranging from 0.028 mg/l to 3.43 mg/l (mean+/-SE, 0.428+/-0.581 mg/l). A retrospective analysis of necropsy reports and archived samples from 15 wild Kea from various South Island locations also was carried out. Seven of these birds (five from the Aoraki/Mount Cook area) died with clinical signs consistent with lead toxicosis and had liver and/or kidney lead levels reported to cause lead toxicity in other avian species. All seven of these birds also had lead inclusions (Ziehl-Neelson positive intranuclear inclusion bodies) in the renal tubular epithelial cells. These are considered diagnostic of lead toxicity in other species. This study showed that lead exposure is ubiquitous in the sampled population and may be an important contributing factor in Kea morbidity and mortality. As a result of these findings, lead abatement in areas frequented by Kea is being initiated.

Lead toxicity in captive and wild Mallards (Anas platyrhynchos) in Spain.

Forty captive Mallards (Anas platyrhynchos), of both sexes, were separated into five groups and dosed with lead shot via oral intubation; one group was used as a control. Lead dosage differed in terms of shot number and size, as well as administration time. One hundred and thirty-five wild mallards were trapped between 1998 and 2001 in the Boada and Nava lagoons near the Canal de Castilla, in the Spanish province of Palencia. Radiologic techniques (ventrodorsal and lateral views) were used to detect lead shot in the gizzard and to determine degradation in dosed birds over time. Heparinized blood samples were taken from wild and captive mallards and blood lead levels were determined using anodic stripping voltammetry with a dropping mercury electrode. Clinical signs, injuries, and body weight were recorded. In approximately 90% of the experimentally dosed mallards, administered shot stayed in their gizzard until it degraded; this took approximately 30 days. Peak lead levels in blood were observed between days 10 and 20, and 10 days following a repeat dosage; males were more sensitive than females to a repeat dosage. During the experimental phase, 34% of birds died, and those that survived had varying degrees of anorexia, lethargy, and a decreased response to external stimulus. Of 135 tested wild mallards, 41% had a blood lead concentration higher than 0.200 microg/g. Lead shot was found embedded in 3.6% of the wild birds and 1.2% had a lead shot pellet in their gizzard.

[Determining factors in lowering blood lead levels below the poisoning threshold in Greater Paris (1992-2006)]. / Déterminants du retour à une plombémie inférieure au seuil d'intoxication en Ile-de-France (1992-2006).

BACKGROUND: Given the serious health effects of lead poisoning (Pb> or =10microg/dL), the present study was designed to estimate the time required to reach and identify factors associated with reaching Pb<10microg/dL according to the severity of the poisoning. METHODS: Since 1992, the Greater Paris lead poisoning monitoring system (SSSILF) has been systematically recording data on blood lead levels of screening and follow-up testing of children in the region. In children under the age of seven when screened positive for lead poisoning, survival curves without reaching the threshold of 10microg/dL and the relative risk (RR) of reaching this threshold were calculated (Kaplan-Meier curves and Cox model), according to blood lead level groups (Group 4: Pb> or =45microg/dL; Group 3: 25microg/dL< or =Pb<45microg/dL; Group 2: 10microg/dL< or =Pb<25microg/dL; (by definition, Group 1: Pb<100microg/L and risk factors of poisoning). RESULTS: The median survival times without reaching the threshold of Pb<10microg/dL were 72.7 months for Group 4, 36.8 months for Group 3 and 14.5 months for Group 2. Compared to reference categories, the time to Pb<10microg/dL was longer for children aged four and over at the time they screened positive for poisoning (Groups 4 and 3), for children displaying pica behavior (Groups 3 and 2), for children in an environment with another child suffering from lead poisoning (Groups 3 and 2) and for children of mothers from Sub-Saharan or North Africa countries (Group 2); the differences reached statistical significance. Changes in Pb levels were better for all children (Groups 4, 3 and 2) screened over the most recent period, i.e. 2002 to 2006, and for Group 2 children living in Paris or the nearby district of Seine-Saint-Denis. CONCLUSION: While the time required has gone down over recent years, the time to reach the threshold of Pb<10microg/dL is counted in years and varies depending on known poisoning risk factors and the district responsible for patient management. It is essential to have early lead poisoning screening for children in high-risk groups and then follow-up after rapid implementation of appropriate medical and social measures.