Midterm 2 Flashcards
top 5 leading causes of death
- dieseas of the heat
- malignant neoplasma
- chronic lower respiratory disease
- cerebrovascular disease (stroke)
- accidents
Disease of the heart + Malignant neoplasms make up… % of deaths
50
women live longer than men but…
their cause of death from stroke or alzheimers disease is higher
top 5 leading causes of deaths for infants
- congenital malformations
- diorders related to short gestation and low birth weight
- suddan infant death syndrome
- newborn affected by maternal complications of pregnancy
- accidents
Death and the environment. 3 kinds of environments that effect
social, geological, biological
example of social environment and death
married, divorced, widowed differnet life expectnacies.
example of geography and death
different areas of the US have different life expectancies
example of biology and death
being male is a risk factor.
1 in 10,000 means
up to one additinal case from a designated cuase in a population of 10,000 people may occur in the next 70years
rate per person-time estimate
example: 10 people exposed to an adgent all worked for different number of yeats. estimate could be X/total of all persons years
estimated relavtive risk
incident rate in exposed/incident rate in non exposed. 1= no association. >1 positive correlation. <negative correlation
de minimis
society must accept some level of risk. threshold below risks are considered trivial. sometimes it is set lower if the benefit is great.
Top 3 underlying causes of death
- tobacco
- poor diet and physical activity
- alcphol consumption
DRI
dietary reference intakes. include EAR, RDA, AI and UL
EAR
estimated average requirment- average intake needed to prevent clinical deficiency
RDA
recommended daily allowance. calculated value (EAR + 2 SD)
AI
adequate intake. in absesnse of data provided an EAR and RDA. Mean intake of a healthy population
UL
upper tolerable level. highest safe intake where no signs of toxicity are evident.
how to estimate when a toxin becomes a hazard
dose response and exposure
NOAEL
No observed adverse effect level- hgighest concentration reported that doesn not cause harm
LOAEL
lowest concentration reporded that does not cause hardm
Estimated Exposure Dose, EED
measured or calculated dose to which humans are likelt to be exposed considering exposure from all other sources and routes.
Margin or exposure, MOE
ratio of the NOAEL and the EED
IPCS
International Programme on Chemical Safety. define “tolerable intake”
Tolerable Intake
lifetime intake of a substanct that can occur without appreciable health risk. TI= NOAEL/UF
UF
uncertainty factor
Interspecies UF
10^0.4 x 10^0.6
Intraspecies UF
10^0.5 x 10^0.5
Boron
widely used in consumer and construction products, an ingrediant in detergents, cosmetics, toothpast, glass and preservatives.
Critical Effect
An observable effect. example: Fetal rat weight. Dont want to chose death as critical effect.
Monitor types
Area monitors, Personnel monitors (radiation badges on indviduals), biomarkers
examples of potential intraspecific differences
fetus or child compared to adult- absorbtion, excretion, metabolism, body burden. male compared to fema, germ cell, developmental toxns. old compared to young- dermal absorption
Reference Dose
replaced the concept of acceptable daily intake to avoide the idea of “acceptabe” and “saftey”. RfD=NOAEL/UF
EPA criteria for evaluating carcinogenic potential
mode of action weight of toxicology evidence dose-response assessment susceptible populations and life-stages evaluation risk from childhood exposures characterizations of overal risk
Mode of Action
sequence of events and processes starting with interaction of an agent with cell. examples: mutagenicity, miogenesis, inhibition of cell death, cytotoxicity
Weight of Evidence
evidence of tumors in exposes animals or humans. chemical and physical properties. evidence hemical activates carcinogenic processes.
Risk assessment Carcinogens
non-caner toxins have threshold. carcinogens to not have thresholds! One moluecule is a risk.
Cancer slope factors
chemical/bodywight per exposure period
Cancer potency
95% upper confidence limit of the slope factor
Cancer risk
C x [(IR x EF e ED)/(BXxAT)]xSFxASF
c=concentration in mg/L IR=intake in L/day BW=body weight EF=exposure frequency ED=exposure duration in years AT=average time exposed SF=cancer slope factor ASF=age senstive factor
Risk Managment
science 30%
Law 30%
Politics 40%
HQ
Hazard Quotient- risk from exposure via a single pathway. EED/RfD
HI
Hazard Index- sum of all HQ
Politics of risk managment
familiar riska are less fearfull. unfamiliar risk are more feared
assessment of microbes
major differences from chemicals:
chemicals do not multiply
microbes multiply and undergo natural selection in host.
neoplasm
tumor
malignant
rapidly growing clones of the cells. cause cachexia(loss of apetite)
Bengign tumors- suffix
-oma. examples: fibroma= benign tumor of fibrous tissue.
carcin-
-oma
malignant tumor of the glands of the stomach
sarc-
-oma
maligmnant tumors of mesenchymal origin
VDPIMP
evaluate biopsy to determin if neoplasm is present
V-variation D-disorganization P-proliferation I-invasion M-metastasis P-persistence
ectoderm=
endoderm=
mesoderm=
carcinoma
carcinoma
sarcoma
Tumors are of monoclonal origin
the cell which initiates genesis of cancer is not itself malignant but the cells progeny
cancer risk is higher in populations exposed to certain chemicals
snuff causes cancer.
chromosomes are involved
chromosomal aberrations are consistently associated with various types of cancer
Ames test
testing for mutagenicity. environmental egents can cuase mutations.
Oncogenes
cancer genes. retroviral RNa0 can reverse transcribe into DNA and incorporant into the host DNA.
proto-oncogene
humans carry genes with that them that when damaged can cause cancer.
- control cell division
- control cell differentiation
- can aquire mutations that convert them into oncogenes
- oncogenes convernt normal cells into cancer cells
types of damage that can convert proto-oncogenes to oncogenes
- point mutations
- translocation
- gene amplification
Tumor suppressor genes
- control cell division
- DNA repair genes
- Apoptosis genes
Normal adult tissue control 3 cell processes
- continued replication
- differentiation to take on specialized functions
- apoptosis
Tissue Cell Number= Cell Proliferation - Cell Death
# of Cells = (oncogenes+damaged tumor suppressor) - damages apoptosis genes ... = CANCER
Familial Proportion of risk
environment plays a bigger role than genetics in cancer.
UV Light and Skin Cancer
UV radiation causes the formation of pyrimadine dimers in specific DNA sequences of the tumor suppressor gene. DNA synthesis will fix these mutations.
Benzo(a)pyrene (BaP)
byproduct of incomplete comustion of coal, wood, tobacco. cuased scrotal cancer in chimney sweeps. protective clohing provided the first successful progrm in cancer prevention.
HPV
the environmental agent in cervical cancer. HPV is very high risk factor for penile, vulvar and cervical cancer. strong link between APV and oral, larynx, esophogus and lung cancer.
Breast Cancer
terminal epithelial milk bulb is wear cancer occurs. ductus system greatly expands when pregnant, even more dense when breast feeding then stops and then apoptosis. becoming pregnant lowers risk for breast cance.r
Stem Cell Cancer Hypothesis
mutations that cause cancer occu in the stem cell or its progenitor cell.
Progenitor Cell
differentiate into different types of specialized cells.
common metals associated with cancer risk
- arsenic
- cadmium
- chromium
- nickel
Genotoxins
agents that cause DNA damage
nucleoside
pyrimidine or purine + ribose
nucleotide
nucleoside + phosphate
Transcription
DNA converted to mRNA
translation
mRNA to protein