Pearl 2014 - Motivating Examples and Transport Formulas
Summary
Three Los Angeles to New York City examples show that the right way to reuse an LA experiment depends on the causal role of the variable Z whose distribution differs between cities. The same observed disparity P(z)=P∗(z) calls for reweighting by P∗(z) when Z is age (Eq. 3.1), for no adjustment when Z is a proxy that does not affect treatment or outcome (Eq. 3.2), and for reweighting by P∗(z∣x) when Z is a post-treatment biomarker (Eq. 3.4).
Overview
Notation used throughout: Π = study population (Los Angeles, experiment available), Π∗ = target population (NYC, only observational data available); starred distributions P∗ refer to Π∗. X = exposure, Y = outcome, Z = covariate. Footnote 11: each graph represents the causal structure of the population prior to treatment, so X is the level of treatment an individual would take by free choice. Footnote 12: the arrow Z→X means older people seek treatment more; Z→Y is the effect of age on the outcome.
Main Content
Example 1: Z = age (Fig. 3a)
An LA randomized trial estimates the age-specific effects P(y∣do(x),Z=z). NYC is older: P(x,y,z)=P∗(x,y,z), in particular P(z)=P∗(z). Natural inclination: age-specific effects are invariant across cities.
Transport formula for pre-treatment Z (Eq. 3.1)
P∗(y∣do(x))=z∑P(y∣do(x),z)P∗(z)(3.1)
It combines experimental results from LA, P(y∣do(x),z), with the observational aspect P∗(z) of NYC to produce an experimental claim about NYC.
Footnote 13: at first glance this is routine “standardization” or “recalibration” (Westergaard 1916; Yule 1934; Lane and Nelder 1982), but it raises the deeper question why age-specific effects should be invariant across populations. The task of the paper: state assumptions that make (3.1) valid. Related questions: what must be assumed about other confounders (latent and observed) for (3.1)? Would the same formula hold if Z were a proxy for age, e.g. language proficiency? What if Z is an exposure-dependent variable such as hypertension level standing between X and Y?
Example 2: Z = language proficiency, a proxy for unmeasured age (Fig. 3b)
Z does not affect X or Y but correlates with both through age, which is unmeasured in both studies. Given P(z)=P∗(z), how to estimate P∗(y∣do(x)) from the z-specific LA effect?
Two readings of the same inequality P(z)=P∗(z):
Reading
What differs
Right formula
(i) Cities have identical age distributions; NYC residents acquire language skills at a younger age, so P(z∣age)=P∗(z∣age)
the mechanism age→Z
P∗(y∣do(x))=P(y∣do(x)) (3.2): Z is irrelevant, ignore the disparity
(ii) P(z∣age)=P∗(z∣age) and the disparity reflects genuine age differences, P(age)=P∗(age)
the age distribution
reweighting is needed, and (3.2) is invalid since age modifies the response to X
Because age is unmeasured, (i) cannot be distinguished from (ii) in the probability distribution P. Every distribution compatible with Fig. 3(b) is also compatible with Fig. 3(a), yet the two processes dictate different transport formulas. Hence “the choice of the proper transport formula depends on the causal context in which population differences are embedded.”
Why Z-specific effects are not invariant here. Using Fig. 3(b), the Z-specific effect in NYC is
If the populations differ in the relation between age and skill, P(age∣z)=P∗(age∣z), the skill-specific causal effect differs as well. Intuition: a NYC person at skill level z is probably in a different age group from a Los Angeles person at the same skill; since age, not skill, shapes treatment response, LA residents respond differently from NYC residents at the same skill. The essential difference between Examples 1 and 2: age is exogenous; skills are indicative of earlier factors (age, education, ethnicity) capable of modifying the effect.
Example 3: Z = post-treatment biomarker, surrogate endpoint (Fig. 3c)
Z is X-dependent, standing on the causal path from X to Y (a disease biomarker); the drug affects Y both directly and through Z; X and Y are confounded. Assume the disparity P(z∣x)=P∗(z∣x) is found, and the z-specific effect P(y∣do(x),z) is estimated in LA for all x,z. Can the (average or z-specific) effect in NYC be estimated?
Here (3.1) is wrong: the overall effect (in LA and NYC) is no longer a simple average of z-specific effects. The correct weighting is
P∗(y∣do(x))=z∑P∗(y∣do(x),z)P∗(z∣do(x))(3.3)
which reduces to (3.1) only when Z is unaffected by X. (3.2) is also wrong because Z lies on the causal path and affects the relation of X and Y.
Surrogate framing. Use Z as a surrogate endpoint for an outcome Y that is expensive to measure (Prentice 1989; Ellenberg and Hamilton 1989). Instead of two locations, take two studies at the same place at different times. In study 1, P(y,z∣do(x)) is measured and Z proves a good surrogate. Once Z is proclaimed a surrogate, manufacturers look for direct means of controlling it (e.g. cholesterol-reducing substances), so both P(z) and P(z∣do(x)) change to P∗(z) and P∗(z∣do(x)). We want the drug effect P∗(y∣do(x)) in the new population as cheaply as possible, by an observational study estimating P∗(z,x), acknowledging confounding between X and Y.
Transport formula for post-treatment Z (Eq. 3.4)
Assuming (graphically) that the disparity stems only from a difference in people’s susceptibility to X (the way Z is affected by X), not from a change in some unobservable confounder,
Footnote 14: often a second randomized experiment to estimate P∗(z∣do(x)) is possible at higher cost; then a transport formula is derivable under more relaxed assumptions, e.g. allowing X and Z to be confounded.
Take-aways from Sec. 3
Transportability is a causal, not statistical, notion (Sec. 4 opening): conditions and formulas depend on causal relations, not only on statistics. In Example 3 it matters whether the change in P(z∣x) was due to a change in how Z is affected by X or due to a change in confounding of X and Z; this cannot be determined by comparing P(z∣x) with P∗(z∣x). If X and Z are confounded (Fig. 6e), P(z∣x)=P∗(z∣x) can hold while P(z∣do(x)) is the same in both, and a different formula emerges.
Licensing transportability requires knowledge of the mechanisms and where they differ.
Summary of the three scenarios: pre-treatment Z, S→Z: use (3.1); unmeasured parent of Z with identical marginals: use (3.2); post-treatment Z, S→Z: use (3.4).
Examples
Numerical check of (3.1) versus the naive carry-over (3.2), and of (3.4)
Toy binary model. Example 1: P(Y=1∣x,z): (0,0):0.20,(1,0):0.50,(0,1):0.30,(1,1):0.40; P(Z=1)=0.30 in LA and 0.70 in NYC. Since Z blocks the backdoor X←Z→Y, P(y∣do(x),z)=P(y∣x,z).
Stratum effects: z=0: +0.30; z=1: +0.10.
LA ATE (also what naive carry-over (3.2) would claim): 0.7(0.30)+0.3(0.10)=0.24.
NYC ATE by (3.1): 0.3(0.30)+0.7(0.10)=0.16.
Example 3: P(Y=1∣x,z)=0.10+0.20x+0.40z, no hidden confounding, P(Z=1∣x)=0.20+0.30x in LA and 0.50+0.10x in NYC. Effect(x:0→1)=0.20+0.40[P(z=1∣x=1)−P(z=1∣x=0)].
LA effect: 0.20+0.40(0.30)=0.32.
NYC effect by (3.4): 0.20+0.40(0.10)=0.24.
Wrongly applying (3.1) with the marginal P∗(z): the z-specific effect is constant at 0.20 so it returns 0.20, missing the mediated part.
p_y = {(0,0):.20,(1,0):.50,(0,1):.30,(1,1):.40} # P(Y=1|x,z) = P(Y=1|do(x),z)ate = lambda pz: sum((p_y[(1,z)]-p_y[(0,z)])*(pz if z else 1-pz) for z in (0,1))print(ate(.30), ate(.70)) # 0.24 (LA / naive), 0.16 (Eq. 3.1 for NYC)p3 = lambda x,z: .10+.20*x+.40*zpzx_tgt = lambda x: .50+.10*xey = lambda x: sum(p3(x,z)*(pzx_tgt(x) if z else 1-pzx_tgt(x)) for z in (0,1))print(ey(1)-ey(0)) # 0.24 (Eq. 3.4)
Marketing reading
Treat “LA experiment, NYC target” as “geo test in market set A, rollout to market set B”. If the markets differ in the share of loyal customers Z (pre-treatment, unaffected by ads), (3.1) says reweight loyalty-specific lifts by the target market’s loyalty mix. If Z is “branded search volume” (reacts to ads), (3.4) says use B’s observedP∗(z∣x) at the spend levels B actually runs. Full discussion: Pearl 2014 - Marketing Application Transporting Geo and Lift Results.