Transient Alterations in Streamwater Quality Induced by Pollution Incidents: Interim Losses Calculations and Compensation Alternatives Based on Habitat Equivalency Analysis.

Pollution incidents cause transient water quality alterations during the passage of contaminants' plume along watercourses, with plume passage period and contaminants' concentrations modelled by advection-dispersion equations. Despite being transient, water quality alterations can impose many impacts on the streamwater ecosystem services. This study proposes two frameworks based on Habitat Equivalency Analysis to be applied during assessments of streamwaters' pollution incidents and respective compensation panoramas: (1) Streamwater interim loss framework, to calculate interim loss debits caused by transient alterations in the streamwater quality; (2) Total credit framework, to calculate streamwater credits generated by improvements in selected watercourse's streamwater quality, produced by wastewater treatment plants in this study. The amount of credits calculated in the selected watercourses assists in the proposal of suitable compensatory remediation projects to offset interim losses. Frameworks' calculations are founded on IVA, a water quality index for protection of aquatic life and aquatic communities. Frameworks' calculations depend on three parameters: IVA, watercourses fluxes and the present value multiplier. The frameworks were calculated in ΔIVAxL, unit defined by multiplying sensed alterations in streamwater quality (as ΔIVA) and streamwater flux, in liters (L). The frameworks were applied to two major streamwater pollution incidents in Brazil, caused by the dam collapses of Mariana and Brumadinho, suggesting suitable compensatory remediations' projects for the respective streamwater interim losses. Depending on the selected project, Brumadinho compensation period varied from 2 to 5 years, with estimated costs in the 2020 Int.$ 5.7-18.7M range; Mariana compensation period varied from 8 to 20 years, with estimated costs in the 2020 Int.$ 16.7-58.1M range. Based on Brumadinho compensatory remediation projects, an average water pollution environmental damage value per interim loss was calculated, 1.17E-4 2020 Int.$/ΔIVAxL, which might be useful in comparing streamwater pollution evaluations around the world.

Testicular dysgenesis syndrome and the estrogen hypothesis: a quantitative meta-analysis: [review] / A síndrome da disgenesia testicular e a hipótese do estrogênio: uma meta-análise quantitativa: [revisão]

Sugeriu-se que anomalias do trato reprodutivo masculino como hipospádia e criptorquidismo, assim como o câncer de testículo, componham uma síndrome comum com diminuição da espermatogênese, e de etiologia comum, a interrupção do desenvolvimento gonadal na fase fetal, a síndrome de disgenesia testicular (SDT). O único levantamento quantitativo da relação entre exposição pré-natal a agentes estrogênicos e câncer de testículo data de mais de dez anos; outras revisões da relação entre compostos estrogênicos diferentes do potente estrogênio sintético dietilstilbestrol (DES) e SDT continuam inconclusivas. Foi feita uma meta-análise quantitativa da relação entre SDT e exposição pré-natal a agentes estrogênicos. A inclusão na análise baseou-se em critérios mecanísticos e foi explorada a plausibilidade de um modo de ação mediada pelo receptor estrogênico-α (REα). Incluíram-se oito estudos sobre a etiologia das hipospádias e/ou criptorquidismo não identificados em revisões sistemáticas anteriores. Mais quatro estudos sobre estrogênios sintéticos resultaram em uma estimativa estatisticamente significativa para câncer de testículo. Os resultados das análises dos subconjuntos apontam à existência de fontes não identificadas de heterogeneidade entre estudos ou populações estudadas.

Male reproductive tract abnormalities such as hypospadias and cryptorchidism, and testicular cancer have been proposed to comprise a common syndrome together with impaired spermatogenesis with a common etiology resulting from the disruption of gonadal development during fetal life, the testicular dysgenesis syndrome (TDS). The only quantitative summary estimate of the link between prenatal exposure to estrogenic agents and testicular cancer was published over 10 years ago; other reviews of the link between estrogenic compounds, other than the potent pharmaceutical estrogen diethylstilbestrol (DES), and TDS end points have remained inconclusive. We conducted a quantitative meta-analysis of the association between the end points related to TDS and prenatal exposure to estrogenic agents. Inclusion in this analysis was based on mechanistic criteria, and the plausibility of an estrogen receptor (ER)-α-mediated mode of action was specifically explored. Eight studies were included, investigating the etiology of hypospadias and/or cryptorchidism that had not been identified in previous systematic reviews. Four additional studies of pharmaceutical estrogens yielded a statistically significant updated summary estimate for testicular cancer. Results of the subset analyses point to the existence of unidentified sources of heterogeneity between studies or within the study population.

Testicular dysgenesis syndrome and the estrogen hypothesis: a quantitative meta-analysis.

Male reproductive tract abnormalities such as hypospadias and cryptorchidism, and testicular cancer have been proposed to comprise a common syndrome together with impaired spermatogenesis with a common etiology resulting from the disruption of gonadal development during fetal life, the testicular dysgenesis syndrome (TDS). The only quantitative summary estimate of the link between prenatal exposure to estrogenic agents and testicular cancer was published over 10 years ago; other reviews of the link between estrogenic compounds, other than the potent pharmaceutical estrogen diethylstilbestrol (DES), and TDS end points have remained inconclusive. We conducted a quantitative meta-analysis of the association between the end points related to TDS and prenatal exposure to estrogenic agents. Inclusion in this analysis was based on mechanistic criteria, and the plausibility of an estrogen receptor (ER)-alpha-mediated mode of action was specifically explored. Eight studies were included, investigating the etiology of hypospadias and/or cryptorchidism that had not been identified in previous systematic reviews. Four additional studies of pharmaceutical estrogens yielded a statistically significant updated summary estimate for testicular cancer. Results of the subset analyses point to the existence of unidentified sources of heterogeneity between studies or within the study population.